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A ketogenic diet and voluntary exercise modify the sciatic nerve and gastrocnemius transcriptome in diet-induced obese mice

ABSTRACT: The metabolic syndrome (MetS), an increasingly prevalent condition, causes peripheral nerve and skeletal muscle damage. Lifestyle interventions, such as a ketogenic diet (KD) and exercise (EX), are recommended to improve MetS and prevent peripheral nerve and skeletal muscle injury. However, a comprehensive understanding of the underlying protective effects of diet and EX on peripheral nerve and skeletal muscle health and a direct comparison of the two is currently lacking. Here, we measured peripheral nerve and skeletal muscle outcomes and examined transcriptomic profiles in the sciatic nerve (SCN) and gastrocnemius muscle (GASTROC) from mice fed standard (SD), 60% high-fat (HFD), or KD. We also evaluated the effect of switching HFD mice to SD, KD, and/or exercise (EX) on SCN and GASTROC. Long-term KD preserved peripheral nerve function while dietary and/or EX interventions improved HFD-induced peripheral neuropathy. Differentially expressed gene analyses followed by mFuzz and pathway enrichment analyses identified alterations in biological processes related to cytoskeletal dynamics, lipid metabolism, and amino acid metabolism by diet or interventions in the SCN and GASTROC. Additionally, diet and interventions led to cell-specific changes within the SCN and GASTROC. Collectively, our findings highlight the importance of a healthy diet and regular EX in promoting peripheral nerve and muscle health. We also highlight new and clinically relevant avenues for therapy.

ORGANISM(S): Mus musculus

PROVIDER: GSE283692 | GEO | 2026/05/27

REPOSITORIES: GEO

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Project description:The underlying mechanism of how the atopic lipids in skeletal muscle affect muscle growth remains elusive. Here we chose miniature Bama swine as our model to mimick human obesity and co-associated metabolic disorders by long time diet induction and study how the atopic fat accumulation in skeletal muscle influence muscle function. After 23 months high-fat high-sucrose diet (HFHSD) fed, the model minipig model of obesity accompanied with metabolic disorders like human, and they had increased body weight and extensive lipids deposition in adipose tissues (AT) and non-AT, especially in skeletal muscle. Further more, the mass of skeletal reduced greatly and the small area (0-2000μm2) muscle reduced after diet induced. The average fiber area of Gastroc reduced 25.2%, but no significant changes appeared in the other skeletal muscles. Antioxidant capacity of skeletal muscle also reduced. Microarray profiles showed genes related to fat deposition promotion (Peroxisome proliferator activated receptor γ, CCAAT/enhancer-binding protein α and apolipoprotein E), muscle growth inhibition (myostatin and p21) up regulated, and some other muscle cell differentiation related genes (myoD) down regulated. Meanwhile, adipokines like adiponectin and 11b-hydroxysteroid dehydrogenase type 1 (11βHSD1) which partake in the crosstalk between AT and skeletal muscles rose up. We draw a clear potential crosstalk pathway that, increased 11βHSD1 secreted by excess AT will promote the expression of the major inhibitor MSTN by activating corticosterone to cortisol, leading to the growth inhibition of skeletal muscle. Overall, this research announces how obesity affects skeletal muscle growth in a crosstalk sight. Male and female Bama minipigs, aged 6 months at the start of the study, were divided into the following two groups for 23 months of treatment. Bama minipigon control (CD group, N=3) were fed standard pig chow. The experimental group (N=6) were fed high-fat high-sucrose diet (53% basal diet, 37% sucrose, 10% lard, HFHSD).

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A ketogenic diet and voluntary exercise modify the sciatic nerve and gastrocnemius transcriptome in diet-induced obese mice

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