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  4. Intravenous Glutamine Administration Improves Glucose Tolerance and Attenuates the Inflammatory Response in Diet-Induced Obese Mice after Sleeve Gastrectomy
 
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Intravenous Glutamine Administration Improves Glucose Tolerance and Attenuates the Inflammatory Response in Diet-Induced Obese Mice after Sleeve Gastrectomy

Journal
Nutrients
Journal Volume
12
Journal Issue
10
Pages
1
Date Issued
2020-10-19
Author(s)
Yeh, Chiu-Li
PO-JEN YANG  
PO-CHU LEE  
JIN-MING WU  
PO-DA CHEN  
CHUN-CHIEH HUANG  
Yeh, Sung-Ling
MING-TSAN LIN  
DOI
10.3390/nu12103192
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/533914
Abstract
Obesity is a health problem associated with many metabolic disorders. Weight reduction can effectively alleviate obesity-associated complications. Sleeve gastrectomy is a commonly used bariatric surgery and is considered safe and effective for improving outcomes. Glutamine (GLN) is an amino acid with anti-oxidative and anti-inflammatory properties. This study used a mouse model of sleeve gastrectomy to investigate the impacts of intravenous GLN administration on glucose tolerance and adipocyte inflammation short-term after surgery. C57BL6 male mice were divided into normal control (NC) and high-fat diet groups. The high-fat diet provided 60% of energy from fat for 10 weeks to induce obesity. Mice fed the high-fat diet were then assigned to a sham (SH) or sleeve gastrectomy with saline (S) or GLN (G) groups. The S group was intravenously injected with saline, while the G group was administered GLN (0.75 g/kg body weight) via a tail vein postoperatively. Mice in the experimental groups were sacrificed on day 1 or 3 after the surgery. Results showed that obesity resulted in fat accumulation, elevated glucose levels, and adipokines production. Sleeve gastrectomy aggravated expressions of inflammatory cytokine and macrophage infiltration markers, cluster of differentiation 68 (CD68), epidermal growth factor-like module-containing mucin-like hormone receptor-like 1 (EMR-1), and macrophage chemoattractant protein-1, in adipose tissues. Treatment of obese mice with GLN downregulated hepatic proteomic profiles associated with the gluconeogenesis pathway and improved glucose tolerance. Moreover, macrophage infiltration and adipose tissue inflammation were attenuated after the sleeve gastrectomy. These findings imply that postoperative intravenous GLN administration may improve glucose tolerance and attenuate inflammation shortly after the bariatric surgery in subjects with obesity.
Subjects
glucose tolerance; glutamine; hepatic proteomic profiles; obesity; sleeve gastrectomy
Glucose tolerance; Glutamine; Hepatic proteomic profiles; Obesity; Sleeve gastrectomy
SDGs

[SDGs]SDG3

Other Subjects
adipocytokine; CD68 antigen; glucose; glutamine; glyceraldehyde 3 phosphate dehydrogenase; hormone receptor; interleukin 1beta; interleukin 6; monocyte chemotactic protein 1; sodium chloride; tumor necrosis factor; autacoid; cytokine; glutamine; adipocyte; adipose tissue; animal cell; animal experiment; animal model; animal tissue; Article; cell infiltration; controlled study; cytokine production; diet-induced obesity; down regulation; gluconeogenesis; glucose level; glucose tolerance; human; inflammation; lipid diet; lipid storage; macrophage; male; mouse; mouse model; nonhuman; protein expression; protein fingerprinting; sleeve gastrectomy; adverse event; animal; C57BL mouse; disease model; drug effect; gastrectomy; glucose tolerance test; inflammation; intravenous drug administration; metabolism; obesity; procedures; Adipose Tissue; Animals; Cytokines; Diet, High-Fat; Disease Models, Animal; Gastrectomy; Gluconeogenesis; Glucose Tolerance Test; Glutamine; Inflammation; Inflammation Mediators; Injections, Intravenous; Macrophages; Male; Mice, Inbred C57BL; Obesity
Type
journal article

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