There are numerous reports on insulin resistance in subjects with hypertriglyceridemia but most of the studies involved obese or diabetic subjects. We were interested to study such events but in a population free from other confounders influencing insulin sensitivity (i.e., obesity, glucose intolerance and hypertension). From the population of a cross-sectional study we obtained 12 subjects with isolated hypertriglyceridemia and compared their insulin sensitivity with that of normolipidemic subjects in that study. Insulin sensitivity and secretory status were computed using homeostasis model assessment (HOMA) software. The insulin sensitivity of hypertriglyceridemic subjects was found to be lower than in normolipidemic subjects. For the hypertriglyceridemic subjects, insulin sensitivity (HOMA%S) was 60.07% (values adjusted for age, BMI, waist circumference, and cholesterol levels), which was substantially lower than that of normolipidemic subjects (150.03%; p<0.001). The insulin secretory status (HOMA%B) of the two groups was 248.17% and 124.63%, respectively, and significantly different (p<0.001). Relative insulin resistance, HOMA-IR, of the two groups was 4.90 and 1.54, respectively. We therefore concluded that in comparison with normolipidemic subjects, the insulin sensitivity of otherwise healthy non-obese hypertriglyceridemic subjects was lower, and that B cells had to work harder to compensate for the lowered insulin sensitivity.
AIM: To determine the effects of lipid lowering by TLC on insulin sensitivity and secretory status of non-obese normoglycemic hyperlipidemic subjects.
METHODS: An intervention study was undertaken on 16 non-obese normoglycemic hyperlipidemic subjects. They underwent 6 months of a TLC regimen. Their insulin sensitivity and lipid status were assessed at baseline and after six months. A control group containing 16 age, sex and body mass index (BMI) matched normolipidemic subjects was also enrolled to compare the change in lipid levels and insulin sensitivity in the hyperlipidemic subjects.
RESULTS: The intervention showed significant reductions in insulin resistance (HOMA-IR reduced from 3.8 to 1.4, p<0.001) and improvement of insulin sensitivity (HOMA%S increased from 50.1% to 121.2%, p=0.004) in hyperlipidemic subjects with associated reductions in lipid levels.
CONCLUSION: Lipid lowering in non-obese hyperlipidemic subjects may be associated with improvement of insulin sensitivity.
Study site: Staff of university and offices, Kelantan, Malaysia
Insulin insensitivity is a common finding in several metabolic disorders including glucose intolerance, dyslipidemia, hyperuricemia and hypertension. Most of the previous studies on insulin sensitivity were performed on diabetic or obese population. So our knowledge about insulin sensitivity of healthy population remains limited. Rising prevalence of obesity, diabetes and metabolic syndrome is a serious issue in Malaysia and some other rapidly developing countries. So it is important to look at the insulin sensitivity status of healthy Malaysian subjects and to compare it in future with those of diabetic, obese or metabolic syndrome patients. In this study we sampled subjects who were independent of confounding factors such as obesity (including abdominal obesity), hypertension and glucose intolerance (diabetes, IGT or IFG) which may influence insulin sensitivity. Fasting plasma glucose, fasting insulin and lipid profile were determined. Insulin sensitivity and secretory status were calculated using the homeostasis model assessment (HOMA) software (HOMA%S, HOMA%B and HOMA-IR). The insulin sensitivity (HOMA%S) of healthy Malay subjects aged between 30-60 years was 155.17%, HOMA-IR was 1.05 and HOMA%B was 116.65% (values adjusted for age, sex, BMI and waist circumference). It was seen that non-obese Malaysians can prevent age related lowering of insulin sensitivity if they can retain their BMI within limit.