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

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

Abstract 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 ri...

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Bibliographic Details
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: US 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
premature coronary artery disease
atherosclerosis
prediabetes
and type 2 diabetes
dyslipidemia
insulin resistance
south Asia
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Summary:Abstract 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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ObjectType-Review-1
ISSN:2472-1972
2472-1972
DOI:10.1210/jendso/bvad167