Tuesday, 29 November 2016

Re: Combining Whey Protein and Cocoa Decreases Spikes in Blood Glucose and Increases Adiponectin Production after Consumption

  • Cocoa (Theobroma cacao, Malvaceae)
  • Whey Protein
  • Lipid and Glucose Metabolism
  • Satiety
Date: 11-15-2016HC# 051633-556

Campbell CL, Foegeding EA, Harris GK. Cocoa and whey protein differentially affect markers of lipid and glucose metabolism and satiety. J Med Food. 2016;19(3):219-227.

Diets consisting of 30% or more calories from protein, and particularly, whey protein, have been shown to be effective in inducing satiety and reducing food intake. The high branched-chain amino acid content, specifically leucine, of whey proteins is associated with inducing satiety. Polyphenols found in cocoa (Theobroma cacao, Malvaceae), fruits, and tea (Camellia sinensis, Theaceae) have been shown to increase satiety, insulin sensitivity, and lipid metabolism. These authors examined the combined health effects of cocoa polyphenolics and whey proteins and aimed to evaluate the effects of these ingredients upon lipid and glucose metabolism and markers of satiety in vitro and in a randomized, single-blind, crossover, clinical trial conducted at North Carolina State University in Raleigh, North Carolina.
In vitro, 3T3-L1 preadipocytes were treated with 0.5-100 µg/mL cocoa polyphenolic extract (CPE) and/or 1-15 mM leucine and assayed for lipid accumulation and leptin production. Leptin is a hormone that increases the feeling of fullness between meals and affects weight management.1 The authors report that cellular lipid accumulation significantly decreased with preadipocyte treatment of 50 µg/mL (35%) and 100 µg/mL (50%) CPE. CPE plus 15 mM leucine reduced lipid accumulation by 22-36%. Leucine treatments of 1 mM to 15 mM significantly increased adipocyte leptin production by 26-37%. Though not statistically significant, CPE treatment of 0.5 µg/mL increased leptin secretion by 25% over a negative control plus solvent.
The effects of leucine upon leptin secretion in this study were not as great as those in previous studies. For example, in earlier studies, adipocyte treatment with 5 mM leucine was reported to increase leptin secretion 2- to 5-fold within 4 hours of treatment.2,3 The reduced effect observed in the current study may be due to the treatment method, say the authors, as complete growth media were supplemented with leucine rather than administering leucine in the absence of most essential nutrients. "Our approach was designed to prevent cellular nutrient starvation and provided a more realistic representation for higher animal studies. However, this approach may have diminished the observed effects of leucine upon leptin secretion," write the authors.
Nine healthy subjects aged between 18 and 35 years participated in the clinical trial, which included 4-hour sessions once weekly for 6 weeks. The subjects were not dieting, had not lost or gained significant weight during the preceding year, had not recently started or ended a regular exercise program, were not allergic to dairy or cocoa ingredients, and had no history of type 1 or type 2 diabetes mellitus.
For each session, the subjects arrived at the laboratory after fasting overnight and completed a baseline hunger questionnaire and underwent a blood draw. They were then randomly assigned to consume 1 of six 340-g beverages, each providing 130-150 calories. The beverages included a placebo (maltodextrin); whey protein isolate (WPI) (donated by Davisco Foods International, Inc.; Le Sueur, Minnesota); Dutch-process low-polyphenolic cocoa (LP) and high-polyphenolic cocoa (HP) (donated by The Hershey Company; Hershey, Pennsylvania); LP+WPI; and HP+WPI. The cocoa-containing beverages LP and HP each provided 36 g cocoa. The subjects ranked beverage liking, provided blood samples to measure glucose and adiponectin levels, and ranked their hunger levels at 0.5, 1, 2, and 4 hours after beverage consumption.
The authors report blood glucose increases compared with baseline with the WPI (8%), HP+WPI (12%), LP+WPI (16%), HP (27%), LP (39%), and placebo (58%) interventions. The WPI intervention significantly lowered glucose levels 30 minutes after consumption (P<0.05). Compared with the LP intervention, HP significantly decreased the 30-minute spike in blood glucose (P<0.05). No significant differences were found between the HP+WPI and LP+WPI interventions. All beverages increased serum adiponectin levels above baseline, except for the placebo beverage, which lowered levels below baseline at all time points after consumption. Adiponectin concentrations peaked between 30 and 60 minutes after consumption. The greatest increases in adiponectin levels were seen with the WPI and HP beverages and were significantly higher than the placebo at 0.5-2 hours and 1 hour after consumption, respectively.
Compared with baseline, all hunger ratings significantly decreased at 30 and 60 minutes after consumption. No significant differences were found in the overall hunger ratings during the 4 hours among beverage treatments. The authors suggest that this lack of differences among treatments was likely due to the limited size of this pilot study, the low calorie content of the beverages, or the use of a robust placebo.
"Overall," state the authors, "our results reinforced those of previous studies: WPI and HP significantly decreased spikes in blood glucose and increased adiponectin production." These findings "indicate that combined cocoa and whey protein consumption may be a potential tool in the formulation of low calorie, satiety-inducing foods."
This study was partially supported by a grant from the Dairy Research Institute (Rosemont, Illinois).
Shari Henson
1Fantuzzi G. Adipose tissue, adipokines, and inflammation. J Allergy Clin Immunol. 2005;115(5):911-919.
2Roh C, Han J, Tzatsos A, Kandror KV. Nutrient-sensing mTOR-mediated pathway regulates leptin production in isolated rat adipocytes. Am J Physiol Endocrinol Metab. 2003;284(2):E322-E330.
3Cammisotto PG, Bukowiecki LJ, Deshaies Y, Bendayan M. Leptin biosynthetic pathway in white adipocytes. Biochem Cell Biol. 2006;84(2):207-214.