دورية أكاديمية
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Impaired Fat Absorption from Intestinal Tract in High-Fat Diet Fed Male Mice Deficient in Proglucagon-Derived Peptides.

التفاصيل البيبلوغرافية
العنوان: Impaired Fat Absorption from Intestinal Tract in High-Fat Diet Fed Male Mice Deficient in Proglucagon-Derived Peptides.
المؤلفون: Nishida K; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Ueno S; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Seino Y; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan.; Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto 604-8436, Japan., Hidaka S; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Murao N; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan.; Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto 604-8436, Japan., Asano Y; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Fujisawa H; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Shibata M; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Takayanagi T; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Ohbayashi K; Laboratory of Animal Science, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan., Iwasaki Y; Laboratory of Animal Science, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan., Iizuka K; Department of Clinical Nutrition, Fujita Health University, Toyoake 470-1192, Japan., Okuda S; Graduate School of Bioscience and Biotechnology, College of Bioscience and Biotechnology, Chubu University, Kasugai 487-8501, Japan., Tanaka M; Graduate School of Bioscience and Biotechnology, College of Bioscience and Biotechnology, Chubu University, Kasugai 487-8501, Japan., Fujii T; Department of Gastroenterology and Hepatology, Fujita Health University, Toyoake 470-1192, Japan.; Department of Medical Research on Prebiotics and Probiotics, Fujita Health University, Toyoake 470-1101, Japan.; BIOSIS Lab. Co., Ltd., Toyoake 470-1192, Japan., Tochio T; Department of Gastroenterology and Hepatology, Fujita Health University, Toyoake 470-1192, Japan.; Department of Medical Research on Prebiotics and Probiotics, Fujita Health University, Toyoake 470-1101, Japan.; BIOSIS Lab. Co., Ltd., Toyoake 470-1192, Japan., Yabe D; Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto 604-8436, Japan.; Center for One Medicine Innovative Translational Research, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.; Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan., Yamada Y; Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto 604-8436, Japan., Sugimura Y; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan., Hirooka Y; Department of Gastroenterology and Hepatology, Fujita Health University, Toyoake 470-1192, Japan.; Department of Medical Research on Prebiotics and Probiotics, Fujita Health University, Toyoake 470-1101, Japan.; BIOSIS Lab. Co., Ltd., Toyoake 470-1192, Japan., Hayashi Y; Department of Endocrinology, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan.; Department of Endocrinology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan., Suzuki A; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake 470-1192, Japan.
المصدر: Nutrients [Nutrients] 2024 Jul 14; Vol. 16 (14). Date of Electronic Publication: 2024 Jul 14.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Publishing Country of Publication: Switzerland NLM ID: 101521595 Publication Model: Electronic Cited Medium: Internet ISSN: 2072-6643 (Electronic) Linking ISSN: 20726643 NLM ISO Abbreviation: Nutrients Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI Publishing
مواضيع طبية MeSH: Diet, High-Fat*/adverse effects , PPAR alpha*/metabolism , PPAR alpha*/genetics , Mice, Knockout* , Lipid Metabolism* , Liver*/metabolism , Proglucagon*/metabolism , Proglucagon*/genetics , CD36 Antigens*/metabolism , CD36 Antigens*/genetics , Intestinal Absorption*, Animals ; Male ; Mice ; Sterol Esterase/metabolism ; Sterol Esterase/genetics ; Triglycerides/metabolism ; Mice, Inbred C57BL ; Fatty Acids, Nonesterified/metabolism ; Glucagon-Like Peptide 1/metabolism ; Duodenum/metabolism ; Carnitine O-Palmitoyltransferase/metabolism ; Carnitine O-Palmitoyltransferase/genetics ; Adipose Tissue/metabolism ; Dietary Fats ; Glucagon-Like Peptide 2/metabolism ; Acyltransferases ; Lipase
مستخلص: (1) Background: Proglucagon-derived peptides (PDGPs) including glucagon (Gcg), GLP-1, and GLP-2 regulate lipid metabolism in the liver, adipocytes, and intestine. However, the mechanism by which PGDPs participate in alterations in lipid metabolism induced by high-fat diet (HFD) feeding has not been elucidated. (2) Methods: Mice deficient in PGDP (GCGKO) and control mice were fed HFD for 7 days and analyzed, and differences in lipid metabolism in the liver, adipose tissue, and duodenum were investigated. (3) Results: GCGKO mice under HFD showed lower expression levels of the genes involved in free fatty acid (FFA) oxidation such as Hsl , Atgl , Cpt1a , Acox1 ( p < 0.05), and Pparα ( p = 0.05) mRNA in the liver than in control mice, and both FFA and triglycerides content in liver and adipose tissue weight were lower in the GCGKO mice. On the other hand, phosphorylation of hormone-sensitive lipase (HSL) in white adipose tissue did not differ between the two groups. GCGKO mice under HFD exhibited lower expression levels of Pparα and Cd36 mRNA in the duodenum as well as increased fecal cholesterol contents compared to HFD-controls. (4) Conclusions: GCGKO mice fed HFD exhibit a lesser increase in hepatic FFA and triglyceride contents and adipose tissue weight, despite reduced β-oxidation in the liver, than in control mice. Thus, the absence of PGDP prevents dietary-induced fatty liver development due to decreased lipid uptake in the intestinal tract.
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معلومات مُعتمدة: 21K11608, 24K14638, 23K24765 Japan Society for the Promotion of Science
فهرسة مساهمة: Keywords: CD36; PPARα; glucagon; high-fat diet; lipid metabolism
المشرفين على المادة: 0 (PPAR alpha)
55963-74-1 (Proglucagon)
0 (CD36 Antigens)
EC 3.1.1.13 (Sterol Esterase)
0 (Triglycerides)
0 (Fatty Acids, Nonesterified)
89750-14-1 (Glucagon-Like Peptide 1)
0 (Ppara protein, mouse)
0 (Cd36 protein, mouse)
EC 3.1.1.3 (PNPLA2 protein, mouse)
EC 2.3.1.21 (Carnitine O-Palmitoyltransferase)
0 (Dietary Fats)
0 (Glucagon-Like Peptide 2)
EC 2.3.- (Acyltransferases)
EC 3.1.1.3 (Lipase)
تواريخ الأحداث: Date Created: 20240727 Date Completed: 20240727 Latest Revision: 20240729
رمز التحديث: 20240729
مُعرف محوري في PubMed: PMC11280123
DOI: 10.3390/nu16142270
PMID: 39064713
قاعدة البيانات: MEDLINE
الوصف
تدمد:2072-6643
DOI:10.3390/nu16142270