On the binding ratio of α-cyclodextrin to dietary fat in humans

KL Catherine Jen,1,2 George Grunberger,3 Joseph D Artiss2,4 1Department of Nutrition and Food Science, Wayne State University, Detroit, MI, USA; 2ArtJen Complexus Inc, Windsor, ON, Canada; 3The Grunberger Diabetes Institute, Bloomfield Hills, MI, USA; 4Department of Pathology, School of Medicine, Wayne State University, Detroit, MI, USA Abstract: &alpha;-Cyclodextrin (&alpha;-CD), a soluble dietary fiber, has been shown to bind and eliminate nine times of its own weight in dietary fat. Studies with different animal models have reported that &alpha;-CD preferentially binds saturated fatty acids, reducing saturated and trans fatty acid levels in blood. A clinical trial demonstrated that &alpha;-CD prevented weight gain in obese diabetic patients. The present study was designed to examine whether &alpha;-CD also shows a preference in binding saturated fatty acids in humans and to confirm the 1:9 binding ratio in humans. Sixty-six obese diabetic patients were recruited at the beginning of this 3-month, double-blind, and placebo-controlled study. Patients were randomly assigned to the Active or Placebo group. Blood samples and 3-day dietary records were collected at baseline and at the end of months 1, 2, and 3. A bottle of 180 tablets of active or placebo tablets was dispensed to each participant at the beginning of each month. Dietary records were analyzed using The Food Processor software. It was observed that &alpha;-CD has a higher affinity towards saturated fats than to unsaturated fats. Participants with higher intakes of total and saturated fat lost more weight than those with lower intakes (P < 0.05 and < 0.01, respectively). These data support the earlier observation in both in vitro and animal studies that &alpha;-CD binds with dietary fat in a 1:9 ratio and further demonstrate the efficacy of &alpha;-CD in binding to and eliminating dietary fat, especially saturated fats. &alpha;-CD may play a significant role in reducing blood cholesterol and triglyceride levels as well as stopping chronic weight gain. Keywords: FBCx&reg;, fat binding capacity, 1:9 binding ratio, reducing blood cholesterol levels, saturated, dietary analysi

High-fat diet combined with low-dose streptozotocin injections induces metabolic syndrome in Macaca mulatta

Metabolic syndrome (MetS) is associated with abdominal obesity, hyperlipidemia, insulin resistance, and type 2 diabetes mellitus, and increases the risk of cardiovascular disease. Given the complex multifactorial pathogenesis of MetS, qualified animal models are currently seriously limited for researchers. The aim of our study was to develop a MetS model in juvenile rhesus monkeys (Macaca mulatta). Rhesus monkeys (1-year-old) fed a high-fat diet (15 % fat, 2 % cholesterol) were used as the HF group (n = 6), and those on a normal diet (5 % fat) were used as the control group (n = 4). After being fed a high-fat diet for approximately 12 months, 2 monkeys (HF + STZ group) were injected with low-dose streptozotocin (STZ, 25 mg/kg) twice, with a 7 days interval, and were then fed the same diet continuously for another 24 months. After 36 months of treatment, the high-fat diet monkeys, including the HF and HF + STZ groups, had acquired increased body weights, abnormal serum lipids, and impaired glucose tolerance compared to the control group. In addition, much more marked metabolic changes were observed in the two monkeys of the HF + STZ group, particularly in terms of high-blood glucose level and insulin resistance. Morphological observation of biopsies of liver and pancreatic tissues showed decreased islet number and mass and decreased insulin staining in the monkeys of the HF + STZ group. In addition, Oil red O staining suggested remarkable accumulation of lipid droplets in the hepatocytes. Our study suggested that a long-term high-fat diet followed with a low-dose STZ was able to induce MetS in juvenile rhesus monkeys with faster pathophysiological progress compared with high-fat diet induction alone. Our primary data showed that this method may have potentials to develop MetS animal model in non-human primates