Our observations are consistent with the hypothesis that energy restriction reduces prostate tumor growth by inhibiting tumor angiogenesis. Furthermore, dietary fat concentration does not influence prostate tumor growth when energy intake is reduced.
Zinc is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant function, growth and reproduction. Many aspects of zinc deficiency-induced anorexia have been well studied in experimental animals, most notably the laboratory rat. There is evidence that suggests zinc deficiency may be intimately involved with anorexia in humans: if not as an initiating cause, then as an accelerating or exacerbating factor that may deepen the pathology of the anorexia. The present review describes recent research investigating the relationship between zinc deficiency and the regulation of food intake, along with advances in the understanding of the food intake and body weight regulation systems. For more comprehensive reviews of zinc nutrition and zinc deficiency, readers are referred to the other reviews in this volume and the review text of Mills (1989). An excellent review focused solely on zinc status and food intake has been presented by O'Dell and Reeves (1989).
The nutritional regulation of intestinal adaptation extends beyond the route of nutrient administration as specific nutrients are known to mediate the adaptive response. Dietary carbohydrates are known to enhance intestinal adaptation in patients with short-bowel syndrome. This review discusses SCFA-induced adaptation in intestinal structure and function in adult rat and neonatal piglet models. Potential mechanisms relate to the salvage of energy as SCFA in the colon, direct mediation of intestinal adaptation by SCFA and stimulated release of glucagon-like peptide-2 (GLP-2) from enteroendocrine L cells by SCFA. Among the produced SCFA, butyrate appears to be responsible for increasing plasma GLP-2 concentration, in addition to the enterotrophic effects. Emerging evidence reveals that physiological concentrations of butyrate acutely upregulate the expression of key enterocyte-associated nutrient transporters. Focused experiments are needed to carefully identify the critical components of intestinal adaptation and yield conclusions regarding the relative contributions of SCFA and GLP-2 during the various phases of this process.
Fructans markedly shifted gut microbiota and improved intestinal physiology in obese mice, but the mechanisms by which they affect gut integrity and inflammation in the obese are still unknown.
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