tse phenomaster environmental chambers (TSE systems)
Structured Review

Tse Phenomaster Environmental Chambers, supplied by TSE systems, used in various techniques. Bioz Stars score: 96/100, based on 856 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/tse phenomaster environmental chambers/product/TSE systems
Average 96 stars, based on 856 article reviews
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1) Product Images from "Pharmacological inhibition of G protein-coupled receptor kinase 5 decreases high-fat diet-induced hepatic steatosis in mice"
Article Title: Pharmacological inhibition of G protein-coupled receptor kinase 5 decreases high-fat diet-induced hepatic steatosis in mice
Journal: Biochemical and biophysical research communications
doi: 10.1016/j.bbrc.2025.153078
Figure Legend Snippet: (A) Study design showing weeks of age and treatment. Six-week-old male C57BL/6J mice were fed a high fat diet (HFD; 45% fat, D12451, Research Diets Inc) for 8 weeks to induce obesity prior to starting water control (open square), 25 mg/kg (closed square) or 50 mg/kg (closed circle) GRK5-IN-2 treatment. After 9 weeks of treatment, metabolic phenotyping started including EchoMRI, intraperitoneal insulin and glucose tolerance tests (IPITT and IPGTT), TSE PhenoMaster chambers, and a lipogenesis functional study. Mice were euthanized after 16 weeks of treatment (Sac). (B) Body weight was measured weekly (n=10/group). (C) Body composition was measured after 9 weeks of treatment (n=10/group). (D-E) After 11–12 weeks of treatment, mice (n=4/group) were used for indirect calorimetry (TSE PhenoMaster System). Uncorrected indirect calorimetry data were analyzed using the CalR web application (version 1.3) with ANCOVA, adjusting for body weight as a covariate. Gray shading indicates a dark cycle. (F-G) Mice (n=10/group) were fasted for 16 and 4 hours in preparation for an IPGTT and IPITT, respectively. Blood glucose was measured at 0, 15, 30, 60, 90, and 120-minutes post injection. Area under the curve (AUC) was calculated to assess glucose and insulin sensitivity. All results are mean ± SEM. Statistical significance was assessed using one-way or two-way ANOVA, followed by Tukey’s multiple comparisons test. Comparisons without p-values are not significant (p > 0.05).
Techniques Used: Control, Functional Assay, Injection
Figure Legend Snippet: (A) Study design illustrating timeline and treatments. Six-week-old male C57BL/6J mice were fed a high-fat diet (HFD; 45% fat, D12451, Research Diets Inc.) for 8 weeks to induce obesity before initiating GRK5-IN-2 treatment. After 9 weeks of treatment, metabolic phenotyping was conducted, including EchoMRI, intraperitoneal insulin (IPITT) and glucose tolerance tests (IPGTT), TSE PhenoMaster metabolic chambers, and a lipogenesis functional assay using radiolabeled tracer. Mice were euthanized after 13 weeks of treatment (Sac). (B) Body weight measured weekly (n=10/group). (C) Body composition assessed via EchoMRI after 9 weeks of treatment (n=10/group). (D) Gonadal white adipose tissue (gWAT) was collected, fixed in 10% formalin, and stained with hematoxylin and eosin (H&E) for histological analysis (n=10/group). Representative H&E-stained gWAT images from water- and GRK5-IN-2-treated mice. (E) Triglyceride (TG) content in gWAT was determined by lipid extraction followed by quantification using a colorimetric assay (n=10/group). (F) RNA was extracted from gWAT (n=10/group), reverse-transcribed to cDNA, and analyzed via real-time PCR to quantify adipogenic and inflammatory gene expression normalized to 18S rRNA (endogenous control). Results are expressed as fold change relative to the water-treated group. All data are presented as mean ± SEM. Statistical significance was assessed using two-tailed Student’s unpaired t test. Comparisons without p-values are not significant (p > 0.05).
Techniques Used: Functional Assay, Staining, Extraction, Colorimetric Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Gene Expression, Control, Two Tailed Test