Premium
A Comparison of Gastric and Jejunal Feeding in Hypercatabolism Associated With Hypothalamic AMPK‐Autophagy‐POMC in Endotoxemic Rats
Author(s) -
Cao Chun,
Li Xiaohua,
Yang Xiaodong,
Xi Fengchan,
Gao Tao,
Xing Chungen,
Yu Wenkui
Publication year - 2020
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1002/jpen.1613
Subject(s) - medicine , endocrinology , ghrelin , ampk , hormone , autophagy , amp activated protein kinase , gastric emptying , protein kinase a , chemistry , stomach , kinase , biochemistry , apoptosis
Abstract Background Hypercatabolism is associated with increased infectious rates and mortality in critically ill patients. Enteral nutrition (EN) is usually used to counteract hypercatabolism. However, the impact of different routes of EN on hypercatabolism remains unknown. Here, we compared the impact of gastric feeding (GF) and jejunal feeding (JF) on gastrointestinal hormones and hypercatabolism, which is associated with hypothalamic adenosine 5′‐monophosphate‐activated protein kinase (AMPK)‐autophagy‐proopiomelanocortin (POMC). Methods Sixty adult male Sprague‐Dawley rats were divided into 5 groups: Sham and lipopolysaccharide (LPS) groups fed a standard chow diet, a pair‐fed group that was a subset of saline‐treated rats pair‐fed with the LPS group, and LPS + JF and LPS + GF groups (received EN via jejunal and gastric tube, respectively, for 3 days [100 kcal/kg/d]). Hypercatabolism was measured by insulin resistance, muscle protein synthesis, and atrophy. Serum gastrointestinal hormones, hypothalamic ghrelin, growth hormone secretagogue receptor‐1α (GHS‐R1α), and AMPK‐autophagy‐POMC markers were also detected. Results GF increased serum total, acylated, desacylated, and hypothalamic ghrelin and decreased glucagon‐like peptide‐1 (GLP‐1). But no effect on pancreatic polypeptide (PYY) and hypothalamic GHS‐R1α was observed. JF showed no effect on hypothalamic ghrelin, GHS‐R1α, and serum total, acylated, and desacylated ghrelin and even further aggravated GLP‐1 and PYY. GF could effectively augment hypothalamic AMPK‐autophagy‐POMC and hypercatabolism. However, JF showed no effect on hypothalamic AMPK‐autophagy‐POMC and hypercatabolism. Conclusions GF could activate hypothalamic AMPK‐autophagy and suppress POMC expression via gastrointestinal hormones to ameliorate hypercatabolism compared with JF, which suggested that GF may be the preferred route of EN in endotoxemic rats.