Effects of Starch-Entrapped Microsphere Supplementation on Metabolic Phenotype in C57BL/6J Mice
Resistant starches are complexes of amylose and/or amylopectin that are indigestible or only partially digestible in the small intestine. When these starches enter the colon, they undergo fermentation via resident bacterial strains to produce the short-chain fatty acids acetate, propionate, and butyrate. Not only does butyrate act as an energy source for colonocytes and regulate luminal pH, but butyrate supplementation has also been demonstrated to confer anti-inflammatory and chemopreventive benefits in cell culture models. Moreover, in murine models of diet-induced obesity and insulin resistance, dietary supplementation of sodium butyrate attenuated weight gain, reduced adipose tissue accumulation, and maintained insulin sensitivity in mice concomitantly fed a high-fat diet. Considering the increasing prevalence of overweight and obesity, estimated to exceed two-thirds of the United States adult population, butyrate has been proposed as a therapeutic candidate to mitigate obesity in humans. Unfortunately, oral sodium butyrate supplementation is not generally feasible in clinical trials due to its unpleasant odor and teratogenic effects at pharmacologic doses. Consequently, current research efforts have been directed toward enhancing endogenous butyrate production in the colon with resistant starch supplementation. These dietary fibers are much better tolerated in the gastrointestinal tract and, because they are present in a variety of foods such as fortified cereals and legumes, can be readily incorporated into the human diet. More recently, a method has been developed to entrap starch within an alginate matrix. These starch-entrapped microspheres (SM) offer greater protection from small intestinal amylases and ferment more slowly in the colon compared to other classes of resistant starches, thereby maintaining butyrate production over a longer time course. In the present study, we assessed the effects of SM supplementation on body weight, body composition, energy intake, energy expenditure, and insulin sensitivity in a mouse model of diet-induced obesity.
Henagan, Purdue University.
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