Targeting insulin resistance with selected antidiabetic agents prevents menopausal associated central obesity, dysglycemia, and cardiometabolic risk.

Abstract

Menopause consequent to reduced circulating estrogen is associated with diminished insulin receptor sensitivity and fat redistribution, particularly central adiposity and increased waist circumference. Peri and menopausal women are at risk of hyperglycemia, prediabetes and attendant metabolic disturbances. Hormone replacement therapy increases insulin receptor sensitivity, but may precipitate an increased cardiovascular risk, depending on the route, if not commenced within the proposed period denoted by the 'timing hypothesis'. The therapeutic ideal of dietary modification with increased physical activity may have compliance issues. We theorize that selected antidiabetic agents reduce visceral fat deposits, restore insulin sensitivity and inhibit inflammatory mediator release. Glucagon-like peptide 1 agonists, sodium-glucose cotransporter 2 inhibitors and even metformin are worthy interventions to treat menopausal-induced obesogenic metabolic conditions. Loss of visceral fat restores insulin receptor sensitivity, decreases central obesity and adipokines to halt dysmetabolic changes.