Reversal of nonalcoholic hepatic steatosis, hepatic insulin resistance, and hyperglycemia by moderate weight reduction in patients with type 2 diabetes.

By K. Petersen, S. Dufour, D. Befroy, M. Lehrke, Rosa Hendler, Gerald I. Shulman. Diabetes, 2005

901 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/823c46790beee8b14128502f7c7e841f6d2ce63f

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Citations in the corpus

A position statement on NAFLD/NASH based on the EASL 2009 special conference. (2010, background): “A modest weight loss results in a significant reduction in liver fat despite minimal reduction in body fat [165,166].”
Non-Alcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases (2017, positive): “Petersen et al. first reported that a moderate caloric restriction ( 1,200 kcal/day) decreased body weight by 10% but was sufficient to reduce hepatic lipid content, normalize hepatic insulin responsiveness, and ‘‘reverse’’ T2D (Petersen et al., 2005).”
Why Does Obesity Cause Diabetes? (2022, background): “…(insulin-mediated suppression of lipolysis) are probably maximally improved with 5%–8% weight loss, whereas greater amounts of weight loss cause a further increase in skeletal muscle insulin sensitivity (insulin-mediated increase in glucose disposal) (Magkos et al., 2016; Petersen et al., 2005).”
Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, positive): “…in liver fat content ( (cid:1) 85%), associated speciﬁcally with a normalization in hepatic insulin sensitivity and reductions in fasting hyperglycemia and hepatic glucose production without changes in intra-myocellular lipid or insulin-mediated whole-body glucose disposal (Petersen et al., 2005).”
Effects of Moderate and Subsequent Progressive Weight Loss on Metabolic Function and Adipose Tissue Biology in Humans with Obesity. (2016, background): “The minimum amount of weight loss needed to increase skeletal muscle insulin sensitivity has been unclear because of conflicting data from different studies reporting either no change or increased insulin-stimulated glucose uptake after 6%–8% weight loss (Kirk et al., 2009; Petersen et al., 2005; Pe”