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Very Low-Calorie Ketogenic Diet (VLCKD) and molecular liver cells modification mediated by Small Extracellular Vesicles (sEVs)

ABSTRACT: The very low-calorie ketogenic diet (VLCKD) has emerged as an effective weight loss strategy for obese patients. It significantly reduces visceral adipose tissue (VAT), which is cardinal for mitigating metabolic complications associated with obesity. By promoting rapid weight loss, VLCKD helps to decrease insulin resistance and alleviate inflammation. Chronic liver inflammation can progress to severe conditions like non-alcoholic steatohepatitis and fibrosis, potentially resulting in liver failure and hepatocellular carcinoma. Transient elastography (FibroScan) is a known technique for assessing hepatic steatosis, with FIB E levels below 8kPa indicating low fibrosis risk (LR), while levels above 8kPa suggest a higher risk of chronic liver disease (IHR). Prevention of fibrosis includes lifestyle changes such as a healthy diet and increased physical activity. Traditional low-calorie diets often fail to achieve significant weight loss; hence, the very low-calorie ketogenic diet (VLCKD) is proposed as an effective strategy to decrease VAT and insulin resistance. Recent studies indicate extracellular vesicles (EVs), particularly small EVs (sEVs), play a crucial role in liver fibrosis by activating hepatic stellate cells. Our group identified that sEVs, to be involved in liver degeneration binded to the fibrosis. The aim of this study is to investigate the role of sEVs in 60 obese adults classified as LR and IHR based on FIB E score, enrolled in an 8-week VLCKD weight loss program. Remarkably, the cellular reactivity to sEVs derived from these patients in the early production and modulation of certain fibrosis markers, such as MMPs, and stress fibres Vimentin, and α-Actin was studied.

ORGANISM(S): Homo sapiens

PROVIDER: GSE279581 | GEO | 2024/12/19

REPOSITORIES: GEO

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Project description:Caloric Restriction in Leptin Deficiency Worsens Myocardial Steatosis: Failure to Upregulate PPAR gamma and Thermogenic Glyecrolipid/Fatty Acid Cycling Growing evidence supports an anti-lipotoxic role for leptin in preventing inappropriate peripheral tissue lipid deposition. Obese, leptin deficient ob/ob mice develop left ventricular (LV) hypertrophy and myocardial steatosis with increased apoptosis and decreased longevity. Here we investigated the cardiac effects of caloric restriction in leptin deficiency. Echocardiography was performed on C57Bl/6 wild-type mice (WT) and 7-month-old ob/ob mice fed ad lib, leptin-repleted (LR-ob/ob), or calorie-restricted (CR-ob/ob) for four weeks. Ventricular tissue was examined by electron microscopy (EM), mitochondrial coupling assay, and microarray expression profiling. LR and CR-ob/ob mice showed decreased body weight, heart weight, and LV wall thickness compared to ad lib ob/ob mice. LV fractional shortening was decreased in ad lib ob/ob mice, but restored to WT levels in LR and CR groups. However, EM revealed severe cardiac steatosis in the CR-ob/ob group compared to only moderate steatosis in ad lib ob/ob . Despite marked cardiac steatosis, CR (like LR) restored mitochondrial coupling to WT levels. CR up-regulated genes associated with oxidative stress and cell death, changes suggestive of cardiac lipotoxicity. LR, but not CR was shown to induce core genes involved in glycerolipid/free fatty acid cycling, a highly thermogenic pathway that can reduce intracellular lipid stores. LR, but not CR up-regulated and restored PGC1 and PPARto wild type levels; CR paradoxically further suppressed cardiac PPAR. Thus, leptin is essential in protecting the heart from lipotoxicity, and the inability to up-regulate the thermogenic glycerolipid/free fatty acid cycling pathway may impair the response of leptin deficient animals to the lipotoxic stress of calorie restriction. 6 month aged ob/ob mice were either leptin repleted with osmotic mini-pumps, calorie restricted to match the caloric intake of the leptin repleted mice, or fed ad lib for one month. 6-8 month C57Bl/6J mice were aged to serve as controls.

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Very Low-Calorie Ketogenic Diet (VLCKD) and molecular liver cells modification mediated by Small Extracellular Vesicles (sEVs)

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