Diet and postprandial risk markers for complications in type 2 diabetes

Abstract

The period after a meal is complex with fluctuation in blood glucose, lipids and other metabolic responses. This may induce and/or increase inflammation and contribute to future development of diabetic complications. Prevention of complications include well-controlled disease management, including diet. There are however gaps in the literature for dietary recommendations in diabetes, and whether those with type 2 diabetes (T2D) make dietary changes. The aims of this doctoral thesis were: 1) To study the acute effects of fructose loading on levels of serum uric acid, metabolic and inflammatory markers using isocaloric drinks; Coca-Cola (17.5 g fructose), blueberry drink (18 g fructose) and a pure fructose drink (35 g fructose), without and with a pizza. 3) To study the acute effect of meals with different compositions of high carbohydrate (HC) (52E%), HC & fibers (50E%, 15 g), low carbohydrate (LC, 32E%)+high fat (HF) (50E%) and LC (28E%)+high protein (HP) (41E%) on metabolic and inflammatory markers 4) Examine possible changes in fruits and vegetables consumption.

The effects of acute fructose loading on levels of serum uric acid were examined in T2D (n=7), chronic kidney disease (n=3) and healthy subjects (HS) (n=6). Serum uric acid increased over time following fructose loading. The highest response was observed following fructose drink, and the lowest following the blueberry drink (p<0.05). The effect of acute fructose loading on glucose, insulin and inflammatory markers were examined in T2D and HS. The response in glucose and insulin was greater following Coca-Cola (p<0.05). MCP-1 decreased in both groups following blueberry drink and Coca-Cola (T2D; p=0.02, HS; p=0.03), probably secondary to the insulin response. The results suggests that drinks with added fructose should be avoided, and that blueberry is protective on uric acid and glucose response.

The effect of meal composition on metabolic and inflammatory markers were examined in T2D and HS. HC meals induced the highest response in glucose and insulin, and LC+HF in triglycerides (p<0.05). The inflammatory marker VCAM-1 decreased following LC+HP meal (T2D; p=0.03, HS; p=0.003), while ICAM-1 decreased following LC+HF (p=0.02) in T2D and following LC+HP (p=0.03) in HS. PAI-1 decreased following HC (T2D; p=0.04, HS; p=0.006) and LC+HP (T2D; p=0.03, HS; p=0.01) and in T2D also following LC+HF (p=0.04). The responses did not differ between meals, probably due to the healthy composition of meals. Thus, LC meals with a healthy composition of fibers, vegetables, berries, mono and poly- unsaturated fat and plant-based proteins could be recommended to subjects with T2D.

Possible changes in intake of fruits and vegetables consumption over time was explored in a prospective cohort of men using food frequency questionnaires in 1997 and 2009. 1 741 men developed T2D and 22 212 remained free from diabetes. Increased intake of fruit and vegetables was greater among those who developed T2D (1.6 servings/week, 95% CI 1.08; 2.03) compared to those remained free from diabetes (0.7 servings/week, 95% 0.54; 0.84). Although improvements in consumption were observed, only 36% of those with T2D consumed ≥5 servings per day in 2009. Thus, there is a need for nutritional education in T2D.