TY - CHAP

T1 - Metabolic Effects of Progressive Weight Loss

AU - Magkos, Faidon

N1 - Publisher Copyright: © 2024 selection and editorial matter, George A. Bray, Claude Bouchard, John Kirwan, Peter Katzmarzyk, Leanne Redman, Philip Schauer; individual chapters, the contributors.

PY - 2024

Y1 - 2024

N2 - The weight loss threshold required for improving metabolic outcomes in obesity and the nature of the dose-response relationship varies by endpoint. Fat mass, fat-free mass, and resting energy expenditure decrease linearly with weight loss. Visceral adipose tissue and liver fat content decrease with small reductions in weight (2-5%), and these reductions continue in a dose-dependent manner. Hepatic inflammation, ballooning, and fibrosis require greater weight loss to improve (≥7-10%). Cardiometabolic risk factors including fasting glucose and insulin concentrations, glycated hemoglobin, lipid profile, and blood pressure improve with small reductions in weight (2-5%), and gradually thereafter with more weight loss, particularly in subjects with greater levels of these risk factors at baseline. Skeletal muscle insulin sensitivity increases dose-dependently from 5% to 16% weight loss, whereas adipose tissue and hepatic insulin sensitivity and hepatic triglyceride secretion improve maximally with modest reductions in weight (5-10%) and do not improve further with more weight loss. Insulin clearance increases after weight loss, whereas pancreatic insulin secretion does not change within the range of weight reduction achieved by most hypocaloric diets (≤16%); but decreases with more weight loss (≥18%). Weight loss dose-dependently reduces the risk of diabetes, reduces the need for antidiabetic medications, and increases chances for diabetes remission. Although there are dose-response relationships for most endpoints, the clinical value of even small amounts of weight loss (2-5%) needs to be stressed before advocating for “more is better.”.

AB - The weight loss threshold required for improving metabolic outcomes in obesity and the nature of the dose-response relationship varies by endpoint. Fat mass, fat-free mass, and resting energy expenditure decrease linearly with weight loss. Visceral adipose tissue and liver fat content decrease with small reductions in weight (2-5%), and these reductions continue in a dose-dependent manner. Hepatic inflammation, ballooning, and fibrosis require greater weight loss to improve (≥7-10%). Cardiometabolic risk factors including fasting glucose and insulin concentrations, glycated hemoglobin, lipid profile, and blood pressure improve with small reductions in weight (2-5%), and gradually thereafter with more weight loss, particularly in subjects with greater levels of these risk factors at baseline. Skeletal muscle insulin sensitivity increases dose-dependently from 5% to 16% weight loss, whereas adipose tissue and hepatic insulin sensitivity and hepatic triglyceride secretion improve maximally with modest reductions in weight (5-10%) and do not improve further with more weight loss. Insulin clearance increases after weight loss, whereas pancreatic insulin secretion does not change within the range of weight reduction achieved by most hypocaloric diets (≤16%); but decreases with more weight loss (≥18%). Weight loss dose-dependently reduces the risk of diabetes, reduces the need for antidiabetic medications, and increases chances for diabetes remission. Although there are dose-response relationships for most endpoints, the clinical value of even small amounts of weight loss (2-5%) needs to be stressed before advocating for “more is better.”.

U2 - 10.1201/9781003432807-33

DO - 10.1201/9781003432807-33

M3 - Book chapter

AN - SCOPUS:85179195581

SN - 9781032551081

SN - 9781032558691

VL - 2

SP - 291

EP - 300

BT - Handbook of Obesity - Volume 2

A2 - Bray, George A.

A2 - Bouchard, Claude

PB - CRC Press

ER -