Effects of a High-Carb vs. High-Fat Meal on Glycemia, Insulin, Interleukin-6, TNF-Alpha, and Apo-B

Abstract

Past studies have shown that food ingestion modulates vascular function within the first two hours of consumption and that food composition such as the amount of carbohydrates vs. fat may play a role. The goal of this study was to assess the effect of a high-carbohydrate (HC) meal vs. a high-fat (HF) meal on potential modulators of vascular function, insulin, interleukin-6 (IL-6), TNF-alfa and Apo-B. We studied a group of healthy volunteers; n=6, age 38 ± 13 years, BMI 24.5 ± 3.8 kg/m2 and systolic blood pressure 125.3 ± 9.1 mmHg. The meals were commercially available; HC meal consisted of 120 gm of carbohydrates (∼60% sugars) and 8 gm fat, and the HF meal consisted of 54 gm of carbohydrates (∼ 15% sugars) and 28 gm of fat and contained slightly (∼20%) less total calories. The meals were ingested within 5 minutes. Results: Glucose and insulin levels increased in response to either meal but more robustly with HC. Glucose and insulin levels peaked at 30 minutes in response to HC and at 60 minutes in response to HF. IL-6 levels nearly doubled in response to either meal, but the time course appeared different; it peaked at 180 minutes and 60 minutes in response to HC and HF, respectively. TNF-alpha levels remained overall unchanged after either HC and HF meal. Apo-B levels also remained overall unchanged after either HC and HF meal. Conclusions: Our study shows that food composition differentially affects the magnitude and time course of changes in metabolites, hormones and markers of inflammation. Ingestion of a HF meal resulted in a delayed and lower peak of glucose and insulin and a much earlier peak in IL-6. This early elevation of IL-6 in response to HF may potentially impair vascular function as described in the “big Mac” study. It is unclear if higher insulin levels during this period would be vaso-protective. Further research is needed to better understand the link between food composition and changes in metabolites, hormones and pro/anti-inflammatory mediators and its relation to vascular function. Disclosure H.O. Steinberg: None. F.B. Stentz: None. N.K. Shankar: None.