Globin digest: no evidence for a weight loss mechanism.
ABSTRACT This study was designed to document the mechanism through which globin digest, a dietary herbal supplement, might cause weight loss by exploring possible fat malabsorption, calorie malabsorption, energy expenditure, and fat oxidation. Six healthy subjects were placed on an outpatient diet for 14 days and given a meal containing 40.9 g of fat on days 5 and 11, and stools were collected for 72 hours after each meal for analysis of fecal fat content. Four grams of globin digest was given with one meal and placebo with the other. In another separate study, six subjects were placed on a 100-g fat, weight-maintaining diet for 14 days. All food was prepared by the Pennington Center (Baton Rouge, LA) metabolic kitchen. Globin digest (2 g) or placebo was given with each of three meals per day, and stool was collected for calorie determinations during the last 72 hours of each week. Subjects received globin digest during one of the 2 weeks and placebo during the other. Resting metabolic rate and respiratory quotient were measured on the last day of each 1-week period. There was no increase in 72-hour fecal fat or fecal calories by bomb calorimetry during either of the studies. There was no difference in the respiratory quotient. Globin digest did result in an increase in resting metabolic rate. However, this increase was not statistically significant. Globin digest, if effective, does not cause weight loss or fat loss through fat malabsorption or a relative increase in fat oxidation. Future studies are needed to document the efficacy of globin digest for weight loss in humans before further mechanistic investigation is attempted.
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ABSTRACT: Globin digest (GD), prepared from globin by acidic protease treatment, suppressed the elevation of serum triglyceride level in not only total but also chylomicron fraction after oral administration of olive oil. By screening with this lowering activity, we concluded that Val-Val-Tyr-Pro (VVYP) would be most effective constituent having hypotriglyceridemic action in GD. The mode of their action was dose dependent and did not show species specificity. Neither the repression of peristaltic movement of intestine nor the delaying of gastric emptying was caused by intake of GD or VVYP, however, the excretion of administered lipid was much more than that of control. Furthermore, administration of GD caused more prominent activation of hepatic triglyceride lipase (HTGL) and the increase of hepatic free fatty acid (FFA) concentration in early phase after administration of fat. From these results, it could be elucidated that GD, and also VVYP, inhibited fat absorption from digestive tract and enhanced activity of HTGL, so that more rapid clearance of dietary hypertriglyceridemia was caused.Life Sciences 02/1996; 58(20):1745-55. · 2.56 Impact Factor