Study summary · research use only
Enteral nutrition alleviated lipopolysaccharides-induced hypercatabolism through ghrelin/GHS-R1α-POMC
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study, researchers examined whether enteral nutrition (EN) alleviates lipopolysaccharide (LPS)-induced hypercatabolism through the ghrelin/GHS-R1α-POMC pathway in endotoxemic rats. Sham and LPS groups had free access to chow and water, while EN, EN+Lys, and EN+3-MA groups received intracerebroventricular injections of saline, D-Lys3-GHRP-6, or 3-MA before three days of EN. Hypercatabolism was assessed via body weight, insulin resistance, leptin, corticosterone, and muscle protein synthesis/atrophy measures, alongside serum and hypothalamic ghrelin, GHS-R1α, and AMPK-autophagy-POMC pathway activity. The abstract reports EN increased ghrelin, acylated ghrelin, and GHS-R1α, activated the hypothalamic AMPK-autophagy-POMC pathway, and was associated with reduced hypercatabolism; these effects were abolished by central D-Lys3-GHRP-6 administration or by 3-MA.
Abstract
Sustained hypercatabolism induced by sepsis contributed to serious complications and mortality in the intensive care unit. Enteral nutrition (EN) was required to maintain the energy balance during sepsis. Ghrelin, which was stimulated secretion by EN, had been shown to regulate energy homeostasis. Therefore, we tested whether EN alleviated hypercatabolism through ghrelin/GH secretagogue receptor 1α (GHS-R1α)-proopiomelanocortin (POMC) in endotoxemic rats. Rats in the Sham and lipopolysaccharide (LPS) groups were free access to rodent chow diet and water. Rats in the EN, EN + Lys and EN + 3-MA groups were intracerebroventricularly injected with saline, D-Lys3-GHRP-6 or 3-MA and then received EN for three days. Hypercatabolism was measured by the change of body weight, insulin resistance, leptin, corticosterone, muscle protein synthesis and atrophy. Serum and hypothalamic total ghrelin, acylated ghrelin, GHS-R1α and AMP-activated protein kinase (AMPK)-autophagy-POMC pathway were also detected. The results showed that EN increased serum and hypothalamic total ghrelin, acylated ghrelin and GHS-R1α, effectively activated the hypothalamic AMPK-autophagy-POMC pathway and alleviated hypercatabolism in endotoxemic rats. The improving effects of EN on hypercatabolism and hypothalamic AMPK-autophagy-POMC pathway were abolished with the central administration of D-Lys3-GHRP-6 to inhibited hypothalamic GHS-R1α. And with the central administration of 3-MA to inhibited hypothalamic autophagy, the improving effect of EN on hypercatabolism was also abolished in endotoxemic rats. In conclusions, EN could significantly alleviate hypercatabolism through ghrelin/GHS-R1α-POMC in endotoxemic rats.
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