metformin hcl Search Results


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Selleck Chemicals metformin
Fig. 4. Inhibition of Complex I sensitized the radioresistant glioma U87MG_F cells to radiation. (A) MTT assay was used to test the effects of rotenone on the growth of U87MG and U87MG_F cells. (B) We used 200 nM rotenone to treat U87MG, U87MG_F and U251 cells. This dose of rotenone does not influence the cell growth. The survivals of cells after treating with rotenone and 2 Gy radiation were analyzed, which showed rotenone can sensitize U87MG_F cells to 2 Gy radiation. However, rote- none did not obviously increase the sensitization of U87MG cells to ra- diation. (C) We used 12 mM <t>metformin</t> treat U87MG, U87MG_F and U251 cells. The survivals of cells after treating with metformin and 2 Gy radiation were analyzed, which showed metformin sensitized U87MG_F cells to 2 Gy radiation. These results demonstrate mitochondria meta- bolism play vital roles in fractioned radiation-induced radioresistance of glioma cells. (D) The Complex I inhibitor, rotenone (200 nM), increases the intracellular ROS production in U87MG and U87MG_F cells, while metformin (12 mM) decrease the ROS production. The ROS in control cells was set 1, and fold changes in the drug-treated cells were shown up. ***p < 0.001.
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Biosynth Carbosynth metformin hydrochloride hcl
Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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Wockhardt limited gliclazide 5 gm
Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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LabCoat Ltd 500 mg metformin hcl osmotic tablets
Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by <t>metformin</t> treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .
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Baseline characteristics of the three intervention groups.
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Image Search Results


Fig. 4. Inhibition of Complex I sensitized the radioresistant glioma U87MG_F cells to radiation. (A) MTT assay was used to test the effects of rotenone on the growth of U87MG and U87MG_F cells. (B) We used 200 nM rotenone to treat U87MG, U87MG_F and U251 cells. This dose of rotenone does not influence the cell growth. The survivals of cells after treating with rotenone and 2 Gy radiation were analyzed, which showed rotenone can sensitize U87MG_F cells to 2 Gy radiation. However, rote- none did not obviously increase the sensitization of U87MG cells to ra- diation. (C) We used 12 mM metformin treat U87MG, U87MG_F and U251 cells. The survivals of cells after treating with metformin and 2 Gy radiation were analyzed, which showed metformin sensitized U87MG_F cells to 2 Gy radiation. These results demonstrate mitochondria meta- bolism play vital roles in fractioned radiation-induced radioresistance of glioma cells. (D) The Complex I inhibitor, rotenone (200 nM), increases the intracellular ROS production in U87MG and U87MG_F cells, while metformin (12 mM) decrease the ROS production. The ROS in control cells was set 1, and fold changes in the drug-treated cells were shown up. ***p < 0.001.

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Inhibition of mitochondria NADH-Ubiquinone oxidoreductase (complex I) sensitizes the radioresistant glioma U87MG cells to radiation.

doi: 10.1016/j.biopha.2020.110460

Figure Lengend Snippet: Fig. 4. Inhibition of Complex I sensitized the radioresistant glioma U87MG_F cells to radiation. (A) MTT assay was used to test the effects of rotenone on the growth of U87MG and U87MG_F cells. (B) We used 200 nM rotenone to treat U87MG, U87MG_F and U251 cells. This dose of rotenone does not influence the cell growth. The survivals of cells after treating with rotenone and 2 Gy radiation were analyzed, which showed rotenone can sensitize U87MG_F cells to 2 Gy radiation. However, rote- none did not obviously increase the sensitization of U87MG cells to ra- diation. (C) We used 12 mM metformin treat U87MG, U87MG_F and U251 cells. The survivals of cells after treating with metformin and 2 Gy radiation were analyzed, which showed metformin sensitized U87MG_F cells to 2 Gy radiation. These results demonstrate mitochondria meta- bolism play vital roles in fractioned radiation-induced radioresistance of glioma cells. (D) The Complex I inhibitor, rotenone (200 nM), increases the intracellular ROS production in U87MG and U87MG_F cells, while metformin (12 mM) decrease the ROS production. The ROS in control cells was set 1, and fold changes in the drug-treated cells were shown up. ***p < 0.001.

Article Snippet: Rotenone and metformin (Selleckchem, USA) was incubated with the cells for 24 h. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) was incubated with the cells for 4 h. Culture medium was removed and 150 μL DMSO (Sangon Inc, China) was added.

Techniques: Inhibition, MTT Assay, Control

Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by metformin treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Maternal HFD intake during lactation leads to excessive maternal weight gain and hyperglycemia at weaning which is not affected by metformin treatment. (A) Schematic representation of experimental design for maternal dietary exposure, treatment interventions and offspring tissue collection at P16 or P21. (B–D) Maternal body weight throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 3–6/group). (E) Maternal body weight gain from P1 to P16 (n = 5–8/group). (F–H) Maternal food intake throughout the lactation period in vehicle-treated, insulin-treated and metformin-treated mothers (n = 4–6/group). (I) Maternal cumulative food intake from P1 to P16 (n = 4–6/group). (J) Maternal random blood glucose levels (mg/dl) at weaning (n = 6–13/group), (K) maternal circulating insulin levels (ng/ml) at weaning (n = 5–8/group), (L) maternal circulating leptin levels (ng/ml) at weaning (n = 6–8/group) and (M) GDF15 plasma levels (pg/ml) at weaning (n = 3–7/group). Light grey shadowed area represents treatment phase, connecting lines represent mean and SEM is represented as colour-specific surrounding fill area (B, C, D, F, G H). In data plotted as box plots (E, I, J) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (K, L, M), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; B, D, F, H), mixed effects model (diet x time; C, G) or 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; E, I, J, K, L). CD/CD: gestational and lactational control diet-fed mothers, CD/HFD: gestational control diet and lactational high-fat diet-fed mothers, HFD/HFD: gestational and lactational high-fat diet-fed mothers, P: postnatal day. Mouse and food icons are from https://scidraw.io/ .

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques: Clinical Proteomics, Derivative Assay, Control

Two-way ANOVA results for <xref ref-type= Figure 1 ." width="100%" height="100%">

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Two-way ANOVA results for Figure 1 .

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques:

Anti-diabetic treatments effects on offspring growth and metabolic hormone levels is dependent on maternal metabolic state. (A–C) Male offspring body weight from vehicle-treated group, from insulin-treated mothers and from metformin-treated group from P4 to P21 (n = 11–14/group). (D) Male offspring body weight at P16 and (E) body weight change from P4 to P16 (n = 16–21/group). (F) Blood glucose levels (n = 18–20/group), (G) insulin, (H) leptin, (I) ghrelin and (J) GDF15 plasma levels in P16 male offspring (n = 5–7/group). (K–M) Female offspring body weight from vehicle-treated group, from insulin-treated mothers and from metformin-treated group from P4 to P21 (n = 10–14/group). (N) Female offspring body weight at P16 and (O) body weight changes from P4 to P16 (n = 16–21/group). (P) Blood glucose levels (n = 7–18/group), (Q) insulin, (R) leptin, (S) ghrelin and (T) GDF15 plasma levels in P16 female offspring (n = 3–7/group). Connecting lines represent mean and SEM is represented as colour-specific surrounding fill area, dotted line indicates P16 time-point (A, B, C, K, L, M). In data plotted as box plots (D, E, N, O) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (F, G, H, I, J, P, Q, R, S, T), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; A, B, C, K, L, M) and 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; D, E, F, G, H, I, J, N, O, P, Q, R, S, T), ##p < 0.01 compared to CD/CD/MET (T). CD/CD: gestational and lactational control diet-exposed, CD/HFD: gestational control diet and lactational high-fat diet-exposed, HFD/HFD: gestational and lactational high-fat diet-exposed.

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Anti-diabetic treatments effects on offspring growth and metabolic hormone levels is dependent on maternal metabolic state. (A–C) Male offspring body weight from vehicle-treated group, from insulin-treated mothers and from metformin-treated group from P4 to P21 (n = 11–14/group). (D) Male offspring body weight at P16 and (E) body weight change from P4 to P16 (n = 16–21/group). (F) Blood glucose levels (n = 18–20/group), (G) insulin, (H) leptin, (I) ghrelin and (J) GDF15 plasma levels in P16 male offspring (n = 5–7/group). (K–M) Female offspring body weight from vehicle-treated group, from insulin-treated mothers and from metformin-treated group from P4 to P21 (n = 10–14/group). (N) Female offspring body weight at P16 and (O) body weight changes from P4 to P16 (n = 16–21/group). (P) Blood glucose levels (n = 7–18/group), (Q) insulin, (R) leptin, (S) ghrelin and (T) GDF15 plasma levels in P16 female offspring (n = 3–7/group). Connecting lines represent mean and SEM is represented as colour-specific surrounding fill area, dotted line indicates P16 time-point (A, B, C, K, L, M). In data plotted as box plots (D, E, N, O) whiskers are min. to max., hinges of boxes are 25th and 75th percentiles, and the middle line is the median. In bar graphs (F, G, H, I, J, P, Q, R, S, T), data are expressed as mean ± SEM with single data points. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 derived from 2-way ANOVA with repeated measures (diet x time; A, B, C, K, L, M) and 2-way ANOVA followed by Tukey's multiple comparisons (diet x treatment; D, E, F, G, H, I, J, N, O, P, Q, R, S, T), ##p < 0.01 compared to CD/CD/MET (T). CD/CD: gestational and lactational control diet-exposed, CD/HFD: gestational control diet and lactational high-fat diet-exposed, HFD/HFD: gestational and lactational high-fat diet-exposed.

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques: Clinical Proteomics, Derivative Assay, Control

Two-way ANOVA results for <xref ref-type= Figure 2 ." width="100%" height="100%">

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Two-way ANOVA results for Figure 2 .

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques:

Metformin does not have an impact on the cell number of the two main arcuate neuronal populations. (A, A′) Representative images of TdTomato-labelled AgRP neurons and their quantification in the mid-portion of the ARH. (B, B′) Representative images of TdTomato-labelled POMC neurons and their quantification in the mid-portion of the ARH. Data are presented as mean ± SEM with single data points. Blue dots represent males and orange dots represent females. Statistical analyses were performed using two-way ANOVA. Scale bar is 100 μm. 3V: third ventricle; ARH: arcuate nucleus of the hypothalamus; CD/CD: gestational and lactational control diet-exposed; CD/HFD: gestational control diet and lactational high-fat diet-exposed; HFD/HFD: gestational and lactational high-fat diet-exposed.

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Metformin does not have an impact on the cell number of the two main arcuate neuronal populations. (A, A′) Representative images of TdTomato-labelled AgRP neurons and their quantification in the mid-portion of the ARH. (B, B′) Representative images of TdTomato-labelled POMC neurons and their quantification in the mid-portion of the ARH. Data are presented as mean ± SEM with single data points. Blue dots represent males and orange dots represent females. Statistical analyses were performed using two-way ANOVA. Scale bar is 100 μm. 3V: third ventricle; ARH: arcuate nucleus of the hypothalamus; CD/CD: gestational and lactational control diet-exposed; CD/HFD: gestational control diet and lactational high-fat diet-exposed; HFD/HFD: gestational and lactational high-fat diet-exposed.

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques: Control

Two-way ANOVA results for <xref ref-type= Figure 5 ." width="100%" height="100%">

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Two-way ANOVA results for Figure 5 .

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques:

Comprehensive analysis of the classical signaling pathway of metformin's mechanism of action in the hypothalamus of P16 male offspring. Relative protein expression of (A) total AMPKα levels, (B) phosphorylated-AMPKα(Thr 172 ) levels and (C) AMPK activation ratio; (D) total LKB1 levels, (E) phosphorylated-LKB1(Ser 428 ) levels and (F) LKB1 activation ratio; (G) total mTOR levels, (H) phosphorylated-mTOR(Ser 2448 ) levels and (I) mTOR activation ratio; and (J) total ACC levels, (K) phosphorylated-ACC(Ser 79 ) levels and (L) ACC activation ratio (n = 6/group). Data are presented as mean ± SEM with single data points. Statistical analyses were performed using two-way ANOVA. CD/CD: gestational and lactational control diet-exposed; CD/HFD: gestational control diet and lactational high-fat diet-exposed; HFD/HFD: gestational and lactational high-fat diet-exposed.

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Comprehensive analysis of the classical signaling pathway of metformin's mechanism of action in the hypothalamus of P16 male offspring. Relative protein expression of (A) total AMPKα levels, (B) phosphorylated-AMPKα(Thr 172 ) levels and (C) AMPK activation ratio; (D) total LKB1 levels, (E) phosphorylated-LKB1(Ser 428 ) levels and (F) LKB1 activation ratio; (G) total mTOR levels, (H) phosphorylated-mTOR(Ser 2448 ) levels and (I) mTOR activation ratio; and (J) total ACC levels, (K) phosphorylated-ACC(Ser 79 ) levels and (L) ACC activation ratio (n = 6/group). Data are presented as mean ± SEM with single data points. Statistical analyses were performed using two-way ANOVA. CD/CD: gestational and lactational control diet-exposed; CD/HFD: gestational control diet and lactational high-fat diet-exposed; HFD/HFD: gestational and lactational high-fat diet-exposed.

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques: Expressing, Activation Assay, Control

Comprehensive analysis of the classical signaling pathway of metformin's mechanism of action in the hypothalamus of P16 female offspring. Relative protein expression of (A) total AMPKα levels, (B) phosphorylated-AMPKα(Thr 172 ) levels and (C) AMPK activation ratio; (D) total LKB1 levels, (E) phosphorylated-LKB1(Ser 428 ) levels and (F) LKB1 activation ratio; (G) total mTOR levels, (H) phosphorylated-mTOR(Ser 2448 ) levels and (I) mTOR activation ratio; and (J) total ACC levels, (K) phosphorylated-ACC(Ser 79 ) levels and (L) ACC activation ratio (n = 6/group). Data are presented as mean ± SEM with single data points. Statistical analyses were performed using two-way ANOVA. CD/CD: gestational and lactational control diet-exposed; CD/HFD: gestational control diet and lactational high-fat diet-exposed; HFD/HFD: gestational and lactational high-fat diet-exposed.

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Comprehensive analysis of the classical signaling pathway of metformin's mechanism of action in the hypothalamus of P16 female offspring. Relative protein expression of (A) total AMPKα levels, (B) phosphorylated-AMPKα(Thr 172 ) levels and (C) AMPK activation ratio; (D) total LKB1 levels, (E) phosphorylated-LKB1(Ser 428 ) levels and (F) LKB1 activation ratio; (G) total mTOR levels, (H) phosphorylated-mTOR(Ser 2448 ) levels and (I) mTOR activation ratio; and (J) total ACC levels, (K) phosphorylated-ACC(Ser 79 ) levels and (L) ACC activation ratio (n = 6/group). Data are presented as mean ± SEM with single data points. Statistical analyses were performed using two-way ANOVA. CD/CD: gestational and lactational control diet-exposed; CD/HFD: gestational control diet and lactational high-fat diet-exposed; HFD/HFD: gestational and lactational high-fat diet-exposed.

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques: Expressing, Activation Assay, Control

Two-way ANOVA results for <xref ref-type= Figure 6 ." width="100%" height="100%">

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Two-way ANOVA results for Figure 6 .

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques:

Two-way ANOVA results for <xref ref-type= Figure 7 ." width="100%" height="100%">

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Two-way ANOVA results for Figure 7 .

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques:

Overview of maternal overnutrition and early metformin exposure effects on the AMPK signaling cascade in the developing hypothalamus of males and females. Maternal overnutrition affected differentially AMPK activation in a sex-specific manner. Early metformin exposure increased phosphorylation of the upstream kinase LKB1 in females, whereas downstream components of AMPK signaling were affected in males. Significant effects of diet exposure or metformin treatment on the phosphorylation of the proteins assessed in the hypothalamus of P16 males (left panel) or P16 females (right panel) are indicated by the black thick arrows. ACC: acetyl-CoA carboxylase; AMPK: AMP-activated protein kinase; LKB1: liver kinase B1; mHFD: maternal high-fat diet; mTORC1: mammalian target of rapamycin complex 1; OCT: organic cation transporter; P: postnatal day; TSC1/2: tuberous sclerosis complex 1/2.

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Overview of maternal overnutrition and early metformin exposure effects on the AMPK signaling cascade in the developing hypothalamus of males and females. Maternal overnutrition affected differentially AMPK activation in a sex-specific manner. Early metformin exposure increased phosphorylation of the upstream kinase LKB1 in females, whereas downstream components of AMPK signaling were affected in males. Significant effects of diet exposure or metformin treatment on the phosphorylation of the proteins assessed in the hypothalamus of P16 males (left panel) or P16 females (right panel) are indicated by the black thick arrows. ACC: acetyl-CoA carboxylase; AMPK: AMP-activated protein kinase; LKB1: liver kinase B1; mHFD: maternal high-fat diet; mTORC1: mammalian target of rapamycin complex 1; OCT: organic cation transporter; P: postnatal day; TSC1/2: tuberous sclerosis complex 1/2.

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques: Activation Assay, Phospho-proteomics

Metformin transporters are expressed in the developing hypothalamus. (A) Oct1 , (B) Oct3 and (C) Mate1 mRNA expression in the hypothalamus across development in wild-type male mice (n = 5–8/time-point). (D) Oct1 , (E) Oct3 and (F) Mate1 mRNA expression in the hypothalamus across development in wild-type female mice (n = 4–10/time-point). Data are expressed as mean ± SEM with single data points in black dots. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 compared to P6, unless indicated. P-values derived from one-way ANOVA followed by Tukey's multiple comparisons. P: postnatal day, W: weeks of age.

Journal: Molecular Metabolism

Article Title: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice

doi: 10.1016/j.molmet.2023.101860

Figure Lengend Snippet: Metformin transporters are expressed in the developing hypothalamus. (A) Oct1 , (B) Oct3 and (C) Mate1 mRNA expression in the hypothalamus across development in wild-type male mice (n = 5–8/time-point). (D) Oct1 , (E) Oct3 and (F) Mate1 mRNA expression in the hypothalamus across development in wild-type female mice (n = 4–10/time-point). Data are expressed as mean ± SEM with single data points in black dots. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 compared to P6, unless indicated. P-values derived from one-way ANOVA followed by Tukey's multiple comparisons. P: postnatal day, W: weeks of age.

Article Snippet: The metformin-treated group consisted of dams receiving metformin hydrochloride (HCl) (#FM25131, Biosynth Carbosynth) into the drinking water (3 mg/ml) and the offspring were daily injected with metformin (200 mg/kg; i.p.), to ensure that they receive a similar dose of metformin as they would get in utero , as previous studies have shown the metformin levels reaching into the pups' circulation through the breast milk are almost undetectable [ ].

Techniques: Expressing, Derivative Assay

Composition of different formulations of  metformin  hydrochloride matrix tablets (∼600 mg tablet).

Journal: Saudi Pharmaceutical Journal : SPJ

Article Title: Development and evaluation of natural gum-based extended release matrix tablets of two model drugs of different water solubilities by direct compression

doi: 10.1016/j.jsps.2015.03.005

Figure Lengend Snippet: Composition of different formulations of metformin hydrochloride matrix tablets (∼600 mg tablet).

Article Snippet: Metformin HCl was a gift from Ernest Chemist Ltd. (Accra, Ghana).

Techniques:

Physical characteristics of  metformin  hydrochloride matrix tablets prepared by direct compression.

Journal: Saudi Pharmaceutical Journal : SPJ

Article Title: Development and evaluation of natural gum-based extended release matrix tablets of two model drugs of different water solubilities by direct compression

doi: 10.1016/j.jsps.2015.03.005

Figure Lengend Snippet: Physical characteristics of metformin hydrochloride matrix tablets prepared by direct compression.

Article Snippet: Metformin HCl was a gift from Ernest Chemist Ltd. (Accra, Ghana).

Techniques:

Swelling index of extended release metformin hydrochloride matrix tablets in phosphate buffer pH 6.8 (mean ± S.D, n = 5).

Journal: Saudi Pharmaceutical Journal : SPJ

Article Title: Development and evaluation of natural gum-based extended release matrix tablets of two model drugs of different water solubilities by direct compression

doi: 10.1016/j.jsps.2015.03.005

Figure Lengend Snippet: Swelling index of extended release metformin hydrochloride matrix tablets in phosphate buffer pH 6.8 (mean ± S.D, n = 5).

Article Snippet: Metformin HCl was a gift from Ernest Chemist Ltd. (Accra, Ghana).

Techniques:

Dissolution profiles of extended release metformin hydrochloride matrix tablets in buffer pH 6.8 (mean ± S.D, n = 3), (a) formulations M1-D6, ST-M, (b) formulations M7-M13, ST-M.

Journal: Saudi Pharmaceutical Journal : SPJ

Article Title: Development and evaluation of natural gum-based extended release matrix tablets of two model drugs of different water solubilities by direct compression

doi: 10.1016/j.jsps.2015.03.005

Figure Lengend Snippet: Dissolution profiles of extended release metformin hydrochloride matrix tablets in buffer pH 6.8 (mean ± S.D, n = 3), (a) formulations M1-D6, ST-M, (b) formulations M7-M13, ST-M.

Article Snippet: Metformin HCl was a gift from Ernest Chemist Ltd. (Accra, Ghana).

Techniques: Dissolution

Release kinetics of  metformin  hydrochloride matrix tablets in phosphate buffer pH 6.8 at 37 °C.

Journal: Saudi Pharmaceutical Journal : SPJ

Article Title: Development and evaluation of natural gum-based extended release matrix tablets of two model drugs of different water solubilities by direct compression

doi: 10.1016/j.jsps.2015.03.005

Figure Lengend Snippet: Release kinetics of metformin hydrochloride matrix tablets in phosphate buffer pH 6.8 at 37 °C.

Article Snippet: Metformin HCl was a gift from Ernest Chemist Ltd. (Accra, Ghana).

Techniques:

Baseline characteristics of the three intervention groups.

Journal: Scientific Reports

Article Title: The Influence of Energy Depletion by Metformin or Hypocaloric Diet on Thyroid Iodine Uptake in Healthy Volunteers: a Randomized Trial

doi: 10.1038/s41598-019-41997-2

Figure Lengend Snippet: Baseline characteristics of the three intervention groups.

Article Snippet: Subjects assigned to the metformin group received metformin (Metformin HCL, Centrafarm B.V., Etten-Leur, The Netherlands) for two weeks, (starting with 500 mg/day, increasing up until 2000 mg/day in the last week).

Techniques: Activity Assay

Effects of hypocaloric dieting and metformin on serum TSH, fT4, T3, rT3, the T3/rT3 ratio and T3/fT4 ratio in healthy volunteers before and after intervention. Serum TSH levels were log transformed and differences before and after intervention were determined with paired student’s T tests. *P < 0.05: significant effect of interventions within groups when compared with baseline.

Journal: Scientific Reports

Article Title: The Influence of Energy Depletion by Metformin or Hypocaloric Diet on Thyroid Iodine Uptake in Healthy Volunteers: a Randomized Trial

doi: 10.1038/s41598-019-41997-2

Figure Lengend Snippet: Effects of hypocaloric dieting and metformin on serum TSH, fT4, T3, rT3, the T3/rT3 ratio and T3/fT4 ratio in healthy volunteers before and after intervention. Serum TSH levels were log transformed and differences before and after intervention were determined with paired student’s T tests. *P < 0.05: significant effect of interventions within groups when compared with baseline.

Article Snippet: Subjects assigned to the metformin group received metformin (Metformin HCL, Centrafarm B.V., Etten-Leur, The Netherlands) for two weeks, (starting with 500 mg/day, increasing up until 2000 mg/day in the last week).

Techniques: Transformation Assay

Effects of hypocaloric dieting and metformin on thyroid iodine-123 (I-123) uptake. Panel A shows the I-123 uptake at 4 hours, 24 hours and 48 hours after ingestion at baseline and after intervention. Panel B shows the percentage of change in I-123 uptake compared to baseline measurements at the three different time points for each intervention. Values are depicted as mean ± SEM.

Journal: Scientific Reports

Article Title: The Influence of Energy Depletion by Metformin or Hypocaloric Diet on Thyroid Iodine Uptake in Healthy Volunteers: a Randomized Trial

doi: 10.1038/s41598-019-41997-2

Figure Lengend Snippet: Effects of hypocaloric dieting and metformin on thyroid iodine-123 (I-123) uptake. Panel A shows the I-123 uptake at 4 hours, 24 hours and 48 hours after ingestion at baseline and after intervention. Panel B shows the percentage of change in I-123 uptake compared to baseline measurements at the three different time points for each intervention. Values are depicted as mean ± SEM.

Article Snippet: Subjects assigned to the metformin group received metformin (Metformin HCL, Centrafarm B.V., Etten-Leur, The Netherlands) for two weeks, (starting with 500 mg/day, increasing up until 2000 mg/day in the last week).

Techniques: