Asian Indian Phenotype (Thin-Fat Asian Indian)

At any body mass index (BMI) and age, Asian Indians have higher body fat, visceral fat and waist circumference (WC); lower skeletal muscle mass; thinner hips; short legs; profoundly higher rates of insulin resistance, metabolic syndrome, diabetes, dyslipidemia hypoadiponectinemia, and increased cardiovascular risk than Europids.1-8 These unique clinical and biochemical characteristics that are commonly found among Asian Indians in particular and South Asians in general are collectively referred to as the “Asian Indian Phenotype” or thin –fat phenotype.9 (Figure 052)

The Asian Indian phenotype fit into the model of metabolically obese, normal weight individuals.10 This group comprises only 6% of all whites but the overwhelming majority of South Asians.6, 11

At comparable levels of total body fat, intra abdominal fat and subcutaneous abdominal fat, Asian Indians have significantly larger adipocytes compared to Europids and is correlated with insulin resistance and adiponectin levels.12

The proclivity for increased visceral fat and insulin resistance is evident even among children aged 8 to 11 years.3, 13, 14 For example, South Asian children with a WC of 80 cm have higher insulin levels than white children with a WC of 90 cm.14

In addition, South Asians also have significant procoagulant tendencies as shown by high plasminogen activator inhibitor-1 and fibrinogen concentrations.15-17 These metabolic abnormalities also contribute to the increased predilection to diabetes and CAD.9

Presence of excess dorsocervical fat (buffalo hump) and excess fat deposit under the chin (double chin) may be used as novel phenotypic markers for insulin resistance and metabolic syndrome among Asian Indians.18, 19

Truncal subcutaneous adiposity measured by subscapular and suprailiac skin fold thickness is more in Asian Indians and correlates with insulin resistant metabolic syndrome.5, 20, 21

Phenotypic differences in obesity and body composition between South Asians and whites are in part responsible for greater metabolic perturbations in the former and have great implications for pathophysiology, management and prevention of obesity–related diseases.3, 5, 13, 14, 22, 23

Sniderman et al24 have proposed the adipose tissue overflow hypothesis to explain the predilection for abdominal obesity, metabolic syndrome and diabetes among South Asians. According to this hypothesis, Asian Indians have very small primary fat depot (the metabolically inert superficial subcutaneous adipose tissue compartment in the lower extremities) compared to Europids.

When energy excess induces obesity, Asian Indians and South Asians rapidly exhaust the storage capacity of their superficial subcutaneous adipose tissue compartment and accumulate fat in the deep subcutaneous tissue and especially the visceral fat depots, before whites do. These secondary adipose tissue compartments are characterized by higher transmembrane fatty acid fluxes resulting in high incidence of dysglycemia, atherogenic dyslipidemia and their product—accelerated vascular disease. 24

This adipose tissue overflow explains the greater cardiometabolic risk in South Asians than in white people at the same absolute adipose tissue body mass.24, 25

Many Asian Indians develop metabolic syndrome and diabetes at BMI <25 kg/m2, which is generally considered normal among whites.9, 26 This also explains why BMI may underestimate the cardiometabolic risk which may be best evaluated by WC or waist-hip ratio.3, 27

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