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Acute Endothelial Benefits of Fat Restriction over Carbohydrate Restriction in Type 2 Diabetes Mellitus: Beyond Carbs and Fats.
Barbosa-Yañez, RL, Dambeck, U, Li, L, Machann, J, Kabisch, S, Pfeiffer, AFH
Nutrients. 2018;10(12)
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The control of type 2 diabetes mellitus has become a global challenge. Cardiovascular disease is a major cause of mortality in type 2 diabetes. The aim of the study is to examine and compare the effect of a hypocaloric very low carbohydrate diet versus hypocaloric low-fat diet on vascular function and visceral adipose tissue in type 2 diabetic patients. The study is a randomised parallel group intervention study with adult type 2 diabetes patients with an age range between 42 and 76 years. Results show that both dietary strategies effectively reduced body weight, total adipose tissue, visceral adipose tissue and lipid accumulation in the liver. However, participants following the low-fat diet experienced greater vascular function enhancements. Authors conclude that low-fat diet elicited advantageous effects on vascular function in patients with type 2 diabetes.
Abstract
BACKGROUND Cardiovascular diseases (CVD) are the major cause of mortality in type 2 diabetes patients (T2DM). The causes are embedded in a complex interplay between excess body fat, insulin resistance and serum lipid anomalies. Endothelial homeostasis is strongly affected by this pathogenic network. Even though metabolic changes and weight loss improve vascular endothelial function, the effect of different dietary approaches is still uncertain for type 2 diabetes patients. OBJECTIVE We aimed to compare the acute effects of a hypocaloric very low carbohydrate (VLC) diet versus a hypocaloric low fat (LF) diet on flow mediated dilation (FMD), intrahepatic lipid (IHL) accumulation and visceral adipose tissue as independent risk factors of CVD in T2DM patients. DESIGN 36 T2DM patients (age 63 ± 8 years, 60% females) were randomly assigned to the VLC diet (4⁻10% of total energy intake (E)) or to the LF diet (<30% E) for 3 weeks. Endothelial function was assessed by the flow mediated dilation (FMD) method. Adipose tissue depots and IHL were determined by magnetic resonance. RESULTS Both dietary strategies reduced body weight, body fat content and IHL. Unexpectedly, the LF group experienced significantly greater enhancement of FMD, compared to the VLC group. The FMD showed a positive correlation with protein intake and fat intake in the LF group, while it revealed a negative correlation with protein intake in the VLC diet group. CONCLUSIONS Reduction of total and hepatic adiposity was shown to be successful using either the VLC or LF hypocaloric diets, however, improvements in FMD may be related to the interplay of fat and protein intake.
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Glycemic load effect on fasting and post-prandial serum glucose, insulin, IGF-1 and IGFBP-3 in a randomized, controlled feeding study.
Runchey, SS, Pollak, MN, Valsta, LM, Coronado, GD, Schwarz, Y, Breymeyer, KL, Wang, C, Wang, CY, Lampe, JW, Neuhouser, ML
European journal of clinical nutrition. 2012;66(10):1146-52
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Dietary intervention studies have shown detrimental metabolic effects of high-glycaemic load diets. The glycaemic index (GI) is the numerical classification of a particular food’s blood glucose-raising effect. The aim of this study was to evaluate the effect of a high-glycaemic load diet on circulating levels of insulin-like growth factor-1 (IGF-1) [hormone] and insulin-like growth factor-binding protein 3 (IGFBP-3) [protein] compared to a low-glycaemic load diet. The study is a randomised controlled crossover study which enrolled 84 normal weight and overweight-obese healthy individuals. The study included two 28-day weight-maintaining high- and low-glycaemic load diets. Results indicate that consumption of a low-glycaemic load diet resulted in lower post-prandial [after a meal] insulin and glucose responses and modestly lower fasting IGF-1 and IGF-1/IGFBP-3 concentrations. However, there were no observable effects of glycaemic load on insulin resistance or glucose-adjusted post-prandial insulin responses in these healthy participants. Authors conclude that further intervention studies are required in order to weigh the impact of dietary glycaemic load on risk for chronic disease.
Abstract
BACKGROUND/OBJECTIVES The effect of a low glycemic load (GL) diet on insulin-like growth factor-1 (IGF-1) concentration is still unknown but may contribute to lower chronic disease risk. We aimed to assess the impact of GL on concentrations of IGF-1 and IGF-binding protein-3 (IGFBP-3). SUBJECTS/METHODS We conducted a randomized, controlled crossover feeding trial in 84 overweight obese and normal weight healthy individuals using two 28-day weight-maintaining high- and low-GL diets. Measures were fasting and post-prandial concentrations of insulin, glucose, IGF-1 and IGFBP-3. In all 80 participants completed the study and 20 participants completed post-prandial testing by consuming a test breakfast at the end of each feeding period. We used paired t-tests for diet component and linear mixed models for biomarker analyses. RESULTS The 28-day low-GL diet led to 4% lower fasting concentrations of IGF-1 (10.6 ng/ml, P=0.04) and a 4% lower ratio of IGF-1/IGFBP-3 (0.24, P=0.01) compared with the high-GL diet. The low-GL test breakfast led to 43% and 27% lower mean post-prandial glucose and insulin responses, respectively; mean incremental areas under the curve for glucose and insulin, respectively, were 64.3±21.8 (mmol/l/240 min; P<0.01) and 2253±539 (μU/ml/240 min; P<0.01) lower following the low- compared with the high-GL test meal. There was no effect of GL on mean homeostasis model assessment for insulin resistance or on mean integrated post-prandial concentrations of glucose-adjusted insulin, IGF-1 or IGFBP-3. We did not observe modification of the dietary effect by adiposity. CONCLUSIONS Low-GL diets resulted in 43% and 27% lower post-prandial responses of glucose and insulin, respectively, and modestly lower fasting IGF-1 concentrations. Further intervention studies are needed to weigh the impact of dietary GL on risk for chronic disease.