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The effects of ketogenic diet on brain gene expressions in type 2 diabetes background

ABSTRACT: Aims: Type 2 diabetes mellitus (T2DM) is considered as a risk of neurodegenerative diseases (NDDs). The ketogenic diet (KD) has significant beneficial effects on glycemic control and may act effectively against NDDs. However, the mechanism by which KD is protective against NDDs is still unknown. In the current study, we aimed to explore a possible interaction of KDs on brain functions by determining the effects of KDs on transcriptional changes of brains in the background of T2DM. Methods: Male db/db mice were fed with KD or normal diet from 9 weeks to 6 months of age, and whole brains were sampled for mRNA-seq analysis. Gene Ontology functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes signaling pathway enrichment analysis were conducted to identify the functions of differentially expressed genes. Proteasomal activities were assessed using biochemical methods. Results: The KD showed significantly beneficial effects on glycemic control and body weight in db/db mice (P < 0.05). Moreover, KD altered gene expressions in multiple pathways including energy metabolism, biosynthesis, and inflammatory responses in the brain of db/db mice. KD improved in db/db mouse brains the proteasome degradation system, the primary quality control machinery whose defects are involved in most NDDs. Conclusions: This study suggests that the KD supplement may activate the expression of genes associated with multiple signaling pathway that are closely involved in NDDs. Our results deepen understanding of the molecular mechanisms underlying the improvement of NDDs with KD intervention and may contribute to the development of promising new therapeutic strategies to NDDs.

ORGANISM(S): Mus musculus

PROVIDER: GSE249467 | GEO | 2024/12/06

REPOSITORIES: GEO

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Project description:We previously reported that a low versus high glycemic index (GI) diet on a high fat (30% kcal fat) background (LGI and HGI, respectively) significantly retarded adverse health effects in C57BL/6J male mice. The LGI diet enhanced whole body insulin sensitivity and repressed high fat diet-induced body and adipose tissue weight gain, resulting in reduced serum leptin and resistin levels (Faseb J 2009; 23: 1092-1101). How white adipose tissue (WAT) is effected is examined in the present study. We characterized the molecular mechanisms underlying the GI-mediated effects in WAT using whole genome transcriptomics technology. We show that a LGI vs. HGI diet mainly exerts its beneficial effects on substrate metabolism, especially insulin signaling of fatty acid metabolism. In addition, cell adhesion and cytoskeleton remodeling showed reduced expression in line with lower WAT mass, but it might also be due to altered insulin sensitivity. An important transcription factor showing enhanced expression is PPARgamma. Furthermore, serum levels of triglycerides, total cholesterol, HDL- and LDL-cholesterol were significantly reduced by a LGI vs. HGI diet, and muscle insulin sensitivity was significantly increased as analyzed by PKB/Akt phosphorylation. Cumulatively, even though these mice were fed a high fat diet, the low versus high GI induced significantly favorable changes in metabolism in WAT. These effects suggest a partial overlap with pharmacological approaches by thiazolidinediones (TZDs) to treat insulin resistance and statins and plantsterols/stanols for hypercholesterolemia. It is therefore tempting to speculate that such a dietary approach might beneficially support pharmacological treatment of insulin resistance or hypercholesterolemia in humans. We analyzed 19 epididymal whie adipose tissue (epiWAT) samples from a 13 week High fat diet, Low glycemic index dietary group (LGI, n=9) versus a High fat diet, High glycemic index dietary group (HGI, n=10) after 13 weeks of feeding wildtype C57BL/6J male adult mice. Of the 19 arrays, we excluded 2 arrays for downstream analysis based on quality control (total final set contains 8 LGI and 9 HGI samples).

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The effects of ketogenic diet on brain gene expressions in type 2 diabetes background

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