Disentangling Dual Threats: Premature Coronary Artery Disease and Early-Onset Type 2 Diabetes Mellitus in South Asians

• Published in: Journal of the Endocrine Society Vol. 8; no. 1; p. bvad167
• Main Authors: Muniyappa, Ranganath, Narayanappa, Satish Babu K
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01.12.2023
• Subjects: Asians; Atherosclerosis; Australia; Bangladesh; Coronary heart disease; Development and progression; Dextrose; Epidemics; Epidemiology; Glucose; Hypertension; Insulin resistance; Lipoprotein A; Low density lipoproteins; Medical research; Medicine, Experimental; Mini-Review; Pakistan; Prediabetic state; Risk factors; South Asia; Type 2 diabetes; Bangladesh; Pakistan; Australia; South Asia; atherosclerosis; premature coronary artery disease; prediabetes; and type 2 diabetes; dyslipidemia; insulin resistance; south Asia
• ISSN: 2472-1972; 2472-1972
• DOI: 10.1210/jendso/bvad167

South Asian individuals (SAs) face heightened risks of premature coronary artery disease (CAD) and early-onset type 2 diabetes mellitus (T2DM), with grave health, societal, and economic implications due to the region's dense population. Both conditions, influenced by cardiometabolic risk factors such as insulin resistance, hypertension, and central adiposity, manifest earlier and with unique thresholds in SAs. Epidemiological, demographic, nutritional, environmental, sociocultural, and economic transitions in SA have exacerbated the twin epidemic. The coupling of premature CAD and T2DM arises from increased obesity due to limited adipose storage, early-life undernutrition, distinct fat thresholds, reduced muscle mass, and a predisposition for hepatic fat accumulation from certain dietary choices cumulatively precipitating a decline in insulin sensitivity. As T2DM ensues, the β-cell adaptive responses are suboptimal, precipitating a transition from compensatory hyperinsulinemia to β-cell decompensation, underscoring a reduced functional β-cell reserve in SAs. This review delves into the interplay of these mechanisms and highlights a prediabetes endotype tied to elevated vascular risk. Deciphering these mechanistic interconnections promises to refine stratification paradigms, surpassing extant risk-prediction strategies.