Young, healthy South Asians have enhanced lipogenic sensitivity to dietary sugar. (16th January 2017)

• Record Type: Journal Article
• Authors: Hudgins, Lisa C.; Hugo, Jonathan L.; Enayat, Samim; Parker, Thomas S.; Artis, Amanda S.; Levine, Daniel M.
• Is Part Of: Clinical endocrinology. Volume 86:Number 3(2017)
• Page Start: 361
• Page End: 366
• Publication Date: 2017-01-16
• Subjects: Endocrinology -- Periodicals; 616.4005
• DOI: 10.1111/cen.13293
• Languages: English
• ISSNs: 0300-0664

Abstract

Summary: Objective: South Asians have higher rates of type 2 diabetes and cardiovascular disease compared to most other racial/ethnic groups. Increased hepatic de novo lipogenesis (DNL) in response to dietary sugar may accelerate the development of these chronic diseases in this population. Study design: Hepatic DNL in response to a calorically sweetened beverage was measured in an outpatient setting in 15 South Asians and 15 Caucasians with similar and normal body mass indexes, waist circumferences, glucose tolerance and lipid profiles. Blood was sampled before and hourly for 4 h after the ingestion of a single beverage made with glucose (1·5 g/kg) and fructose (1·5 g/kg). The main outcome, DNL, was measured as the increase in %palmitate (16:0) in very low‐density lipoprotein (VLDL) triglyceride (TG) over 4 h. Results: After the sugar dose, the increase in %16:0 in VLDL TG was significantly greater in South Asians vs Caucasians ( P = 0·01). VLDL and total TG also increased to a significantly greater extent in South Asians ( P = 0·04 and <0·001, respectively). Although the fasting and postsugar levels of insulin and glucose did not differ between groups, the DNL response significantly correlated with the insulin response to sugar in South Asians ( r = 0·56, P = 0·03). Conclusions: Hepatic DNL in response to a sugar challenge was greater in healthy, young South Asians compared to Caucasians despite normal indices of insulin sensitivity, and it correlated with the insulin response. These findings suggest an early, insulin‐related, gene–nutrient interaction contributing to the high prevalence of diabetes and coronary disease in this population.