Islets RNA-seq from male C57Bl/6J on ketogenic diet
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PROVIDER: PRJNA1114063 | ENA |
REPOSITORIES: ENA
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Project description:A ketogenic diet (KD) is a very low-carbohydrate, very high-fat diet recently proposed to treat obesity and type 2 diabetes. While KD grows in popularity, its effects on metabolic health are understudied. (here) We show that, while KD protects against weight gain and induces weight loss, over long-term, mice develop hyperlipidemia, hepatic steatosis, and severe glucose intolerance. Unlike HFD-fed mice, KD mice are not insulin resistant and have low levels of insulin. Hyperglycemic clamp and ex vivo GSIS revealed cell-autonomous and whole-body impairments in insulin secretion. Major ER/Golgi stress and disrupted ER-Golgi protein trafficking was indicated by transcriptomic profiling of KD islets and confirmed by electron micrographs showing a dilated and fragmented Golgi network compatible with defects in insulin granule biogenesis and secretion. Overall, our results suggest long-term KD leads to multiple aberrations of metabolic parameters that caution its systematic use as a health promoting dietary intervention.
2025-08-18 | GSE268020 | GEO
Project description:Liver RNA-seq from male C57Bl/6J on a ketogenic diet
| PRJNA1043181 | ENA
Project description:A ketogenic diet (KD) is a very low-carbohydrate, very high-fat diet recently proposed to treat obesity and type 2 diabetes. While KD grows in popularity, its effects on metabolic health are understudied. (here) We show that, while KD protects against weight gain and induces weight loss, over long-term, mice develop hyperlipidemia, hepatic steatosis, and severe glucose intolerance. Unlike HFD-fed mice, KD mice are not insulin resistant and have low levels of insulin. Hyperglycemic clamp and ex vivo GSIS revealed cell-autonomous and whole-body impairments in insulin secretion. Major ER/Golgi stress and disrupted ER-Golgi protein trafficking was indicated by transcriptomic profiling of KD islets and confirmed by electron micrographs showing a dilated and fragmented Golgi network compatible with defects in insulin granule biogenesis and secretion. Overall, our results suggest long-term KD leads to multiple aberrations of metabolic parameters that caution its systematic use as a health promoting dietary intervention
2025-08-18 | GSE248297 | GEO
Project description:Increased fat intake is associated with obesity and insulin resistance. In some individuals, a failure of pancreatic b-cells to increase insulin production in response to the high demands of obesity leads to diabetes. We sought to determine whether the impaired b- cell adaptation in obesity is associated with differential expression of genes involved in b-cell expansion and intermediary metabolism. Two strains of inbred mice prone to obesity, C57Bl/6J and AKR/J, were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57Bl/6J mice on regular rodent chow or high fat diet. Insulin secretion was 3.2 fold higher in AKR/J than C57Bl/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4 fold greater in AKR/J compared with C57Bl/6J. To elucidate the factors associated with the differences in insulin, we analyzed the gene expression profiles in pancreatic islets in AKR/J and C57Bl/6J mice. Of 14,000 genes examined, 220 were up-regulated and 286 were down-regulated in islets from diet-induced obese AKR/J mice compared with C57Bl/6J mice. Key genes involved in islet signaling and metabolism, e.g. glucagon like peptide-1 receptor, sterol Co-A desaturase 1 & 2 and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function. Keywords: response to high fat diet
2008-02-28 | GSE10639 | GEO
Project description:Male C57Bl/6J mice were fed 45%kcal fat diet (HF) or regular rodent chow (NC) from 4 weeks to 16 weeks of age. Gene expression was compared between RNA obtained from pancreatic islets of HF fed mice and NC mice.
2011-11-20 | GSE23325 | GEO
Project description:Increased fat intake is associated with obesity and insulin resistance. In some individuals, a failure of pancreatic b-cells to increase insulin production in response to the high demands of obesity leads to diabetes. We sought to determine whether the impaired b- cell adaptation in obesity is associated with differential expression of genes involved in b-cell expansion and intermediary metabolism. Two strains of inbred mice prone to obesity, C57Bl/6J and AKR/J, were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57Bl/6J mice on regular rodent chow or high fat diet. Insulin secretion was 3.2 fold higher in AKR/J than C57Bl/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4 fold greater in AKR/J compared with C57Bl/6J. To elucidate the factors associated with the differences in insulin, we analyzed the gene expression profiles in pancreatic islets in AKR/J and C57Bl/6J mice. Of 14,000 genes examined, 220 were up-regulated and 286 were down-regulated in islets from diet-induced obese AKR/J mice compared with C57Bl/6J mice. Key genes involved in islet signaling and metabolism, e.g. glucagon like peptide-1 receptor, sterol Co-A desaturase 1 & 2 and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function. Experiment Overall Design: Microarray analyses were performed on quadruplicate RNA samples of pancreatic islets from AKR and Bl6 mice placed on high-fat diet for 3 months. Pancreases from two mice were combined to yield one sample of islet RNA. All protocols were conducted as described in the Affymetrix GeneChips Expression Analysis Technical Manual (Affymetrix, Santa Clara, CA) using 5 μg total RNA and GeneChip Mouse Expression Arrays MOE 430 (Affymetrix).
2008-04-07 | E-GEOD-10639 | biostudies-arrayexpress
Project description:Analysis of liver gene transcription during feeding of a ketogenic diet. Ketogenic diets may alter physiologic and metabolic profiles in a direction that favors weight loss. C57BL/6J mice were maintained for six weeks on either chow or ketogenic diet. Mice eating KD had lower weights, 90% reduction in insulin levels and increased energy expenditure compared to animals fed chow. Despite consumption of a very high fat diet serum lipids remained normal. Here we show that consumption of KD shifted liver metabolism to drastically increased fatty acid oxidation. Concurrently, expression of genes involved in fatty acid synthesis were markedly suppressed. Reference: A high fat, ketogenic diet induces a unique metabolic state in mice. Kennedy AR, Pissios P, Out H, Xue B, Asakura K, Furukawa N, Marino FE, Liu FF, Kahn BB, Liberman TA, Maratos-Flier E. in press, 2007, Am J Physiol Metab 292. Experiment Overall Design: Eight week old C57BL/6 mice were fed either chow (Labdiet 5008, Pharmserv) or KD (F3666, Bio-Serv) for six weeks. Livers were harvested in the morning in ad lib fed animals. Total RNA from 2-3 animals in each group was used for Affymetrix analysis.
2007-12-13 | E-GEOD-7699 | biostudies-arrayexpress
Project description:Analysis of liver gene transcription during feeding of a ketogenic diet. Ketogenic diets may alter physiologic and metabolic profiles in a direction that favors weight loss. C57BL/6J mice were maintained for six weeks on either chow or ketogenic diet. Mice eating KD had lower weights, 90% reduction in insulin levels and increased energy expenditure compared to animals fed chow. Despite consumpiton of a very high fat diet serum lipids remained normal. Here we show that consumption of KD shifted liver metabolism to drastically increased fatty acid oxidation. Concurrently, expression of genes involved in fatty acid synthesis were markedly suppressed. Keywords: Hepatic profile
2007-05-04 | GSE7699 | GEO
Project description:Specific pathogen free wild-type C57Bl/6 male mice fed ketogenic diet (Bio-Serv AIN-76-A) for 4 weeks Keywords: RNA Expression Array Hearts from 12 week-old mice that were maintained on a standard polysacchardide-rich chow until the age of 8 weeks, at which time they were switched to a ketogenic diet (ad libitum) and maintained for 4 additional weeks prior to collection of tissues
2010-06-16 | E-GEOD-21368 | biostudies-arrayexpress
Project description:Total proteome from sorted primary intestinal epithelial cells isolated from the small intestines of 4 C57Bl/6J mice
2024-10-02 | PXD055546 | Pride