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NCT ID: NCT06334666 Not yet recruiting - Metabolic Syndrome Clinical Trials

The Efficacy of Pedometer-motivated Physical Activity for the Management of Patients With MASLD.

Start date: April 1, 2024
Phase: N/A
Study type: Interventional

The study conducted a health survey among Thai adults in 2022 and found a significant increase in obesity and nonalcoholic fatty liver disease (NAFLD), leading to metabolic-associated steatotic liver disease (MASLD). The prevalence of NAFLD was 19.7%, with higher rates in individuals with metabolic syndrome and diabetes. MASLD is associated with insulin resistance and genetic polymorphisms, particularly the patatin like phospholipase domain containing 3-rs738409 variant. Additionally, physical activity was inversely related to liver disease risk, with higher step counts associated with reduced incidence of NAFLD and liver-related mortality. The study aims to investigate the impact of dietary advice and pedometer use on physical activity levels and health outcomes in MASLD patients over 24 weeks.

NCT ID: NCT01945671 Not yet recruiting - BMI Clinical Trials

The Influence of Obesity on Oocyte, Cumulus and Granulosa Functioning

Start date: November 2013
Phase: N/A
Study type: Observational

Obese women have a higher prevalence of infertility than their lean counterparts. Obesity is a risk factor for anovulation , including in response to gonadotropin treatment .Further, even in women who are cycling regularly, obesity is associated with increased time-to-pregnancy and decreased chance of natural pregnancy. During obesity or periods of overnutrition, lipid accumulates in nonadipose tissues, notably skeletal muscle, liver, heart, and pancreas due to cellular uptake of exogenous fatty acids, triglycerides, and cholesterol as well as de novo lipogenesis in response to elevated glucose. The accumulation of intracellular lipid leads to high levels of free fatty acids that are subject to oxidative damage and the formation of cytotoxic and highly reactive lipid peroxides, which ultimately are detrimental to intracellular organelles, particularly the endoplasmic reticulum (ER) and mitochondria. Exposure of the ER to high levels of free fatty acids and lipid peroxides causes structural alterations that perturb ER function and lead to accumulation of unfolded proteins and calcium release. Failure of the UPR to reestablish ER homeostasis can lead to apoptosis .When mitochondria are exposed to high levels of free fatty acids, these can become oxidized by mitochondrial reactive oxygen species, forming lipid peroxides that damage essential proteins and uncouple mitochondrial function. This results in mitochondrial damage, which can cause further accumulation of lipids that cannot be catabolized, disrupted cellular homeostasis, and ultimately apoptosis . The cellular mechanisms by which obesity causes decreased conception rates are not known. Based on extensive evidence of obesity-induced lipotoxicity in other cells, it was hypothesized that obesity results in the activation of lipotoxicity pathways in the ovary. It was shown that lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis occur in ovarian cells and the oocyte in response to a high-fat diet. The aim of our study was to evaluate the influence of high BMI on oocytes, granulose cells and metabolites in the follicular fluid.