Nutritional evaluation of α-cyclodextrin using canine, hamster, and in vitro models

α-CYCLODEXTRIN;alpha-cyclodextrin;cyclodextrin, fat, digestibility, in vitro fermentation;microbiota;cholesterol;serum lipid profiles;fat absorption;bile acids;HMG-CoA reductase;7 alpha-hydroxylase (CYP7A1)

Guevara Zubillaga, Marcial A.

关键词: α-CYCLODEXTRIN;    alpha-cyclodextrin;    cyclodextrin, fat, digestibility, in vitro fermentation;    microbiota;    cholesterol;    serum lipid profiles;    fat absorption;    bile acids;    HMG-CoA reductase;    7 alpha-hydroxylase (CYP7A1);   

Others  :  https://www.ideals.illinois.edu/bitstream/handle/2142/29583/GuevaraZubillaga_Marcial.pdf?sequence=1&isAllowed=y

美国|英语

来源: The Illinois Digital Environment for Access to Learning and Scholarship

【 摘 要 】

The main objective of this research was to characterize the nutritional effects of α-cyclodextrin (ACD) using in vitro, canine, and hamster models. Study 1 evaluated the composition of ACD, validated select fat analysis techniques as related to ACD-fat complexes, and evaluated the gastrointestinal tolerance, total tract nutrient digestibility, and blood lipid profiles of dogs as affected by ACD supplementation. Hydrolysis of ACD showed that it is effectively composed only of glucose. The acid hydrolyzed fat (AHF) method proved to be valid for measuring fat bound to ACD. Intake of ACD was shown to be generally well tolerated by dogs and did not alter body weight (BW), body condition scores (BCS), or fecal scores. Intake of 6 or 12 g ACD daily decreased apparent nutrient digestibility and numerically reduced serum cholesterol concentrations in hypercholesterolemic dogs, but failed to reduce serum cholesterol concentrations in normocholesterolemic dogs. Study 2 evaluated in vitro fermentation characteristics of α-, β-, and γ-cyclodextrins, and in vivo total tract and ileal nutrient digestibilities, fecal microbiota concentrations, and blood lipid profiles of dogs as affected by ACD supplementation. Maximal in vitro production of total SCFA was lowest for ACD. However, the greatest maximal production of propionate also was noted for ACD. Average daily food intake, BW gain, BCS, and ileal nutrient digestibility were not significantly different among treatments. Total tract nutrient digestibility and fecal dry matter (DM) concentration decreased linearly for treatment groups receiving ACD. Fecal output expressed on an as-is basis, on a DM basis, and on an as-is per g DM intake basis increased linearly (P<0.05) with increasing ACD supplementation. Bifidobacteria, Clostridium perfringens, and E. coli concentrations were not different among treatments. Serum cholesterol and triglyceride concentrations were within normal ranges for dogs and were not different among treatments. Study 3 evaluated apparent nutrient digestibility, cecal SCFA concentrations, cecal microbiota concentrations, blood lipid profiles, bile acid excretion, and liver gene expression of hamsters as affected by ACD and cholesterol intakes. Fecal bile acid excretion was increased by cholesterol intake, but not by ACD intake. Cecum and cecal content weight were increased by ACD intake, whereas cholesterol intake tended to decrease (P=0.08) cecal content weigh expressed on a DM basis. Intake of ACD alone resulted in higher propionate concentrations in cecal contents. Total CFU of lactobacilli and total microbes in cecal contents were greater for hamsters fed ACD than for those not fed ACD. Intake of diets containing ACD tended to increase (P=0.10) expression of 7 α-dehydroxylase(CYP7A1), whereas intake of diets containing cholesterol resulted in a reduction in expression ofhydroxymethylglutaryl (HMG)-CoA reductase. α-Cyclodextrin intake resulted in reduced cholesterol concentrations in serum of normocholesterolemic hamsters, but failed to reduce cholesterol concentrations in dietary-induced hypercholesterolemic hamsters. In summary, ACD intake varied in its ability to affect cholesterol metabolism, nutrient digestibility, fecal characteristics, and hindgut microbiota and fermentation patterns. This variation in response is due to differences in the model used to evaluate it, inclusion level in diet, and matrix where it is supplied. The hypocholesterolemic effect of ACD appears to be a combination of factors including up-regulation of cholesterol degradation through CYP7A1, changes in hindgut fermentation profiles, and, perhaps, changes in hindgut microbiota. However, further research is necessary to define the mechanisms for such up-regulation and microbiota effects on bile acid degradation and excretion.