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gestational diabetes mellitus  (Galectin Therapeutics)

 
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    Galectin Therapeutics gestational diabetes mellitus
    Gestational Diabetes Mellitus, supplied by Galectin Therapeutics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/gestational+diabetes+mellitus/pmc12937688-10-15-0
    Average 86 stars, based on 1 article reviews
    gestational diabetes mellitus - by Bioz Stars, 2026-09
    86/100 stars

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    other:

    Article Title: Intratumoral Collinsella aerofaciens exhibits antitumor activity in endometrial carcinoma through activation of the p53 signaling pathway.
    Article Snippet: A closer look at Galectin-3: its association with 904 gestational diabetes mellitus revealed by systematic review and meta-analysis.

    Article Title: Assessment of Serum Galectin-3 Levels in Patients with Gestational Diabetes Mellitus
    Article Snippet: Keywords: Galectin‐3, gestational diabetes mellitus, subclinical inflammation

    Expressing:

    Article Title: Galectins: Role and Therapeutics in Diabetes and Diabetic Foot Ulcers
    Article Snippet: Galectin-1 [ , , , , ] , Adipose Tissue, Pancreatic β-cells, Renal Tubular Cells , Accelerates high-fat diet (HFD)- induced obesity and lipogenesis; negatively associated with fasting glucose; enhances glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells; elevated levels are associated with lower renal function. , Promotes adipogenesis by interacting with and activating PPARγ transcriptional activity (adipose tissue); deficiency results in reduced expression of lipogenic genes (adipose tissue); enhances β-cell insulin release (paracrine effect); promotes kidney fibrosis via the Akt/AP4 signaling pathway under hyperglycemia.. .. Galectin-2 [ , ] , Placenta, Cardiovascular Tissue , Placental expression is often upregulated in Gestational Diabetes Mellitus (GDM); genetic variants are linked to elevated fasting glucose and insulin levels. , Genetic polymorphisms (SNP rs7291467) in the encoding gene (LGALS2) correlate with higher fasting levels of glucose and insulin; they may influence M1 macrophage polarization.. .. Galectin-3 [ , , , , , , ] , Macrophages, Adipocytes, Hepatocytes, Myocytes, Pancreatic β-cells , Causes systemic Insulin Resistance and glucose intolerance; elevated in obesity, T2DM, prediabetes, and GDM; contributes to β-cell apoptosis (when overexpressed in β-cells); may promote glycolysis. , Extracellular Gal-3 directly binds the Insulin Receptor (InsR), inhibiting tyrosine phosphorylation and downstream signaling (IRS1/AKT); intracellular Gal-3 acts as an LPS sensor to activate the mTORC1 pathway, promoting glycolysis (upregulating GLUT1, HK2, PKM2); secreted Gal-3 impairs β-cell function by inhibiting calcium channels (CACNG1)..



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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in <t>gestational</t> diabetes mellitus <t>(GDM).</t> During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.
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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in <t>gestational</t> diabetes mellitus <t>(GDM).</t> During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.
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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in <t>gestational</t> diabetes mellitus <t>(GDM).</t> During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.
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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in <t>gestational</t> diabetes mellitus <t>(GDM).</t> During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.
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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in <t>gestational</t> diabetes mellitus <t>(GDM).</t> During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.
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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in <t>gestational</t> diabetes mellitus <t>(GDM).</t> During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.
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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in <t>gestational</t> diabetes mellitus <t>(GDM).</t> During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.
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    Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in gestational diabetes mellitus (GDM). During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.

    Journal: Frontiers in Microbiology

    Article Title: Gut microbiota-derived short-chain fatty acids attenuate placental ferroptosis and insulin resistance in gestational diabetes via the ACSL4/LPCAT3 pathway

    doi: 10.3389/fmicb.2026.1715392

    Figure Lengend Snippet: Schematic of the proposed mechanism by which the gut microbiota-placenta axis regulates trophoblast ferroptosis in gestational diabetes mellitus (GDM). During a healthy pregnancy (left panel), a normobiotic gut microbiota produces abundant short-chain fatty acids (SCFAs). These microbial metabolites suppress ferroptosis in placental trophoblasts by upregulating the key antioxidant enzyme glutathione peroxidase 4 (GPX4) and downregulating the pro-ferroptotic enzymes Acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3). This action preserves placental health and supports a normal pregnancy outcome. Conversely, in the GDM state (right panel), gut microbiota dysbiosis leads to a significant deficiency in SCFAs. The lack of SCFAs results in the disinhibition of ferroptosis in trophoblasts, characterized by the downregulation of GPX4 and upregulation of ACSL4 and LPCAT3. This molecular shift facilitates the peroxidation of polyunsaturated fatty acids (PUFAs), culminating in trophoblast ferroptosis, placental injury, inflammation, and contributing to the pathophysiology of GDM.

    Article Snippet: The gestational diabetes mellitus (GDM) model was induced on gestational day (GD) 0 by a single intraperitoneal injection of streptozotocin (STZ; MedChemExpress, #HY-13753, Shanghai, China) at a dose of 40 mg/kg dissolved in 0.1 M citrate buffer (pH 4.5) after overnight fasting ( ).

    Techniques:

    Proposed mechanism by which gut microbiota-derived short-chain fatty acids (SCFAs) protect against gestational diabetes mellitus (GDM)-induced placental ferroptosis. (Left panel) In the healthy state, SCFA-producing bacteria in the gut microbiota generate acetate, propionate, and butyrate, which enter the bloodstream and reach placental trophoblast cells. (Center panel) Within placental trophoblast cells, SCFAs regulate two opposing pathways: (1) Protective pathway (green box): SCFAs upregulate glutathione peroxidase 4 (GPX4) expression, which reduces lipid hydroperoxides (LOOH) to lipid alcohols (LOH), thereby preventing lipid peroxidation and maintaining membrane integrity. (2) Harmful pathway (red box): SCFAs suppress the expression of acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3), thereby preventing the activation and incorporation of polyunsaturated fatty acids [PUFAs, including arachidonic acid (AA) and adrenic acid (AdA)] into membrane phospholipids, which would otherwise be vulnerable to peroxidation. (Right panel) In the GDM/dysbiosis state, reduced SCFA production disrupts this protective mechanism. Downregulation of GPX4 impairs the antioxidant defense, while upregulation of ACSL4 and LPCAT3 promotes PUFA incorporation into membrane phospholipids. The resulting accumulation of lipid peroxides triggers ferroptosis and subsequent placental injury. SCFAs, short-chain fatty acids; GDM, gestational diabetes mellitus; GPX4, glutathione peroxidase 4; ACSL4, acyl-CoA synthetase long-chain family member 4; LPCAT3, lysophosphatidylcholine acyltransferase 3; PUFAs, polyunsaturated fatty acids; AA, arachidonic acid; AdA, adrenic acid; LOOH, lipid hydroperoxide; LOH, lipid alcohol.

    Journal: Frontiers in Microbiology

    Article Title: Gut microbiota-derived short-chain fatty acids attenuate placental ferroptosis and insulin resistance in gestational diabetes via the ACSL4/LPCAT3 pathway

    doi: 10.3389/fmicb.2026.1715392

    Figure Lengend Snippet: Proposed mechanism by which gut microbiota-derived short-chain fatty acids (SCFAs) protect against gestational diabetes mellitus (GDM)-induced placental ferroptosis. (Left panel) In the healthy state, SCFA-producing bacteria in the gut microbiota generate acetate, propionate, and butyrate, which enter the bloodstream and reach placental trophoblast cells. (Center panel) Within placental trophoblast cells, SCFAs regulate two opposing pathways: (1) Protective pathway (green box): SCFAs upregulate glutathione peroxidase 4 (GPX4) expression, which reduces lipid hydroperoxides (LOOH) to lipid alcohols (LOH), thereby preventing lipid peroxidation and maintaining membrane integrity. (2) Harmful pathway (red box): SCFAs suppress the expression of acyl-CoA synthetase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3), thereby preventing the activation and incorporation of polyunsaturated fatty acids [PUFAs, including arachidonic acid (AA) and adrenic acid (AdA)] into membrane phospholipids, which would otherwise be vulnerable to peroxidation. (Right panel) In the GDM/dysbiosis state, reduced SCFA production disrupts this protective mechanism. Downregulation of GPX4 impairs the antioxidant defense, while upregulation of ACSL4 and LPCAT3 promotes PUFA incorporation into membrane phospholipids. The resulting accumulation of lipid peroxides triggers ferroptosis and subsequent placental injury. SCFAs, short-chain fatty acids; GDM, gestational diabetes mellitus; GPX4, glutathione peroxidase 4; ACSL4, acyl-CoA synthetase long-chain family member 4; LPCAT3, lysophosphatidylcholine acyltransferase 3; PUFAs, polyunsaturated fatty acids; AA, arachidonic acid; AdA, adrenic acid; LOOH, lipid hydroperoxide; LOH, lipid alcohol.

    Article Snippet: The gestational diabetes mellitus (GDM) model was induced on gestational day (GD) 0 by a single intraperitoneal injection of streptozotocin (STZ; MedChemExpress, #HY-13753, Shanghai, China) at a dose of 40 mg/kg dissolved in 0.1 M citrate buffer (pH 4.5) after overnight fasting ( ).

    Techniques: Derivative Assay, Bacteria, Expressing, Membrane, Activation Assay