12/7/2023 0 Comments Alpha sigma alpha utsaKaur A, Patankar JV, de Haan W, Ruddle P, Wijesekara N, Groen AK, Verchere CB, Singaraja RR, Hayden MR, Loss of Cyp8b1 improves glucose homeostasis by increasing GLP-1, Diabetes 64 (2015) 1168–1179.Alpha Sigma Alpha is a women’s organization that exists to promote high ideals and standards for its members throughout their lives by emphasizing balance among the four aims of intellectual, physical, social and spiritual development. Woollett LA, Buckley DD, Yao L, Jones PJH, Granholm NA, Tolley EA, Tso P, Heubi JE, Cholic acid supplementation enhances cholesterol absorption in humans, Gastroenterology 126 (3) (2004) 724–731.īertaggia E, Jensen KK, Castro-Perez J, Xu Y, Di Paolo G, Chan RB, Wang L, Haeusler RA, Cyp8b1 ablation prevents Western diet-induced weight gain and hepatic steatosis because of impaired fat absorption, Am J Physiol Endocrinol Metab. Ishida H, Noshiro M, Okuda K, Coon MJ, Purification and characterization of 7alpha-hydroxy-4-cholesten-3-one 12alpha-hydroxylase, J. Murakami K, Okada Y, Okuda K, Purification and characterization of 7alpha-hydroxy-4-cholesten-3-one 12alpha-monooxygenase, J. A p-value of <0.05 was considered a significant difference. Group differences were compared using one-way analysis of variance (ANOVA) or two-way ANOVA followed by Tukey’s multiple comparisons tests. Baseline, before drug treatment Recovery, 14 days of wash-out phase after 1st drug treatment 2nd treatment, after 7 days of drug treatment IP-inhibitor (n = 3), HFHS/IR mice treated with the inhibitor, indicated by a closed square (■) IP-vehicle (n = 2), HFHS/IR mice treated with the vehicle, indicated by a closed circle. (E) GTT AUC showed each treatment period. (D) 2 days after 2nd drug treatment, glucose clearance was improved with drug treatment (IP-inhibitor) compared to the vehicle-treated group. (C) Final body weight was not different between groups. (B) Food intake during 2nd drug treatment was not different. Drug treatment with TE vehicle increased body weight. 1st treatment of drug/vehicle with IP injection decreased body weight despite the mice were fed a HFHS, but during the 2 weeks of recovery, mice gained body weight. (A) % BW changes during the study period. IR: mice that developed insulin resistance without obesity.Įffect of drug treatment on body weight, food intake, and glucose handling with 2nd drug treatment. OB: mice that developed insulin resistance with obesity. A p-value of < 0.05 was considered a significant difference. HFHS/UT (n = 8), mice fed with a high-fat and a high-sucrose diet (HFHS) only, indicated by closed diamond (◆) OG-vehicle (n = 2), HFHS/OB mice treated with vehicle, indicated by a closed triangle (▲) OG-inhibitor (n = 3), HFHS/OB mice treated with the inhibitor, indicated by a closed reversed triangle IP-inhibitor (n = 3), HFHS/IR mice treated with the inhibitor, indicated by a closed square (■) IP-vehicle (n = 2), HFHS/IR mice treated with the vehicle, indicated by a closed circle. IP, intraperitoneal injection OG, oral gavage. BW, body weight GTT AUC, the area under the curve of glucose tolerance test. (D) GTT AUC did not change in either the drug treatment or vehicle treatment. (B)-(C) Food intake was altered by the drug delivery method. (A) Body weight (BW) decreased after 7 days of treatment. Published by Elsevier Inc.Įffect of drug treatment on body weight, food intake, and glucose handling with 1st drug treatment. Taken together, these promising results will lead to a P450 8B1 inhibitor as a potential therapeutic strategy to treat obesity-associated insulin resistance.īile acids Cytochrome P450 8B1 Inhibitor Organic synthesis Pyridine.Ĭopyright © 2021. Seven days of new inhibitor treatment showed attenuation of glucose intolerance in mice that were fed a high fat and a high sucrose diet (HFHS) without affecting body weight. The synthesis of a rationally designed inhibitor for P450 8B1 was achieved through the incorporation of a C12-pyridine in the C-ring of a steroid molecule. Cholic acid is the 12α-hydroxylated bile acid implicated in enhanced absorption of cholesterol. P450 8B1 is the enzyme that hydroxylates its substrate, 7α-hydroxy-cholest-4-en-3-one to 7α-,12α-dihydroxycholest-4-en-3-one, which ultimately results in the formation of cholic acid. Thus, the inhibition of P450 8B1 is a target to treat obesity-associated metabolic disorders. Mice that lack the gene for expression of cytochrome P450 8B1 (P450 8B1) resist weight gain and improve glucose tolerance when fed a high-fat diet.
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