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

被引：3

作者：

Nishida, Koki ^{[1
,2
,3
]}

Ueno, Shinji ^{[1
,2
,3
]}

Seino, Yusuke ^{[1
,2
,3
,4
]}

Hidaka, Shihomi ^{[1
,2
,3
]}

Murao, Naoya ^{[1
,2
,3
,4
]}

Asano, Yuki ^{[1
,2
,3
]}

Fujisawa, Haruki ^{[1
,2
,3
]}

Shibata, Megumi ^{[1
,2
,3
]}

Takayanagi, Takeshi ^{[1
,2
,3
]}

Ohbayashi, Kento ^{[5
]}

Iwasaki, Yusaku ^{[5
]}

Iizuka, Katsumi ^{[6
]}

Okuda, Shoei ^{[7
]}

Tanaka, Mamoru ^{[7
]}

Fujii, Tadashi ^{[8
,9
,10
]}

Tochio, Takumi ^{[8
,9
,10
]}

Yabe, Daisuke ^{[4
,11
,12
]}

Yamada, Yuuichiro ^{[4
]}

Sugimura, Yoshihisa ^{[1
,2
,3
]}

Hirooka, Yoshiki ^{[8
,9
,10
]}

Hayashi, Yoshitaka ^{[13
,14
]}

Suzuki, Atsushi ^{[1
,2
,3
]}

机构：

[1] Fujita Hlth Univ, Dept Endocrinol, Sch Med, Toyoake 4701192, Japan

[2] Fujita Hlth Univ, Dept Diabet, Sch Med, Toyoake 4701192, Japan

[3] Fujita Hlth Univ, Metab, Sch Med, Toyoake 4701192, Japan

[4] Kansai Elect Power Med Res Inst, Yutaka Seino Distinguished Ctr Diabet Res, Kyoto 6048436, Japan

[5] Kyoto Prefectural Univ, Grad Sch Life & Environm Sci, Lab Anim Sci, Kyoto 6068522, Japan

[6] Fujita Hlth Univ, Dept Clin Nutr, Toyoake 4701192, Japan

[7] Chubu Univ, Coll Biosci & Biotechnol, Grad Sch Biosci & Biotechnol, Kasugai 4878501, Japan

[8] Fujita Hlth Univ, Dept Gastroenterol & Hepatol, Toyoake 4701192, Japan

[9] Fujita Hlth Univ, Dept Med Res Prebiot & Probiot, Toyoake 4701101, Japan

[10] BIOSIS Lab Co Ltd, Toyoake 4701192, Japan

[11] Gifu Univ, Ctr One Med Innovat Translat Res, Grad Sch Med, Gifu 5011194, Japan

[12] Kyoto Univ, Grad Sch Med, Dept Diabet Endocrinol & Nutr, Kyoto 6068507, Japan

[13] Nagoya Univ, Res Inst Environm Med, Dept Endocrinol, Nagoya 4648601, Japan

[14] Nagoya Univ, Dept Endocrinol, Grad Sch Med, Nagoya 4668550, Japan

来源：

NUTRIENTS | 2024年 / 16卷 / 14期

基金：

日本学术振兴会;

关键词：

high-fat diet; glucagon; PPAR alpha; CD36; lipid metabolism; GLUCAGON RECEPTOR; HEPATIC STEATOSIS; ADIPOSE-TISSUE; PPAR-ALPHA; INSULIN; METABOLISM; CD36; CHOLESTEROL; LIPOPROTEIN; HOMEOSTASIS;

D O I：

10.3390/nu16142270

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

(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 Ppar alpha (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 Ppar alpha 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 beta-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.

引用

页数：21

共 63 条

[1] Dual elimination of the glucagon and GLP-1 receptors in mice reveals plasticity in the incretin axis [J].