Study summary · research use only
GHSR signalling in perinatal phases is involved in liver metabolism at puberty
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in rats examined the contribution of growth hormone secretagogue receptor (GHSR) signalling during perinatal phases to neurodevelopment and energy metabolism, using LEAP2[1-14] injections in pregnant female rats and postnatal modulation with LEAP2[1-14] or MK677. Perinatal GHSR modulation by LEAP2[1-14] affected glucose homeostasis in a sex- and phase-dependent manner without altering body weight gain or food intake, and liver PEPCK expression was reported to be notably affected by LEAP2 injections. The authors state perinatal LEAP2 exposure can modulate liver metabolism and systemic glucose homeostasis, and suggest these results may represent early signs of later metabolic imbalance, though describing the effects as not pronounced.
Abstract
Ghrelin has effects that range from the maturation of the central nervous system to the regulation of energy balance. The production of ghrelin increases significantly during the first weeks of life. Studies have addressed the metabolic effects of liver-expressed antimicrobial peptide 2 (LEAP2) in inhibiting the effects evoked by ghrelin, mainly in glucose homeostasis, insulin resistance, and lipid metabolism. Despite the known roles of ghrelin in the postnatal development, little is known about the long-term metabolic influences of modulation with the endogenous expressed growth hormone secretagogue receptor (GHSR) inverse agonist LEAP2. This study aimed to evaluate the contribution of GHSR signalling during perinatal phases, to neurodevelopment and energy metabolism in young animals, under inverse antagonism by LEAP2[1-14]. For this, two experimental models were used: (i) LEAP2[1-14] injections in female rats during the pregnancy. (ii) Postnatal modulation of GHSR with LEAP2[1-14] or MK677. Perinatal GHSR modulation by LEAP2[1-14] impacts glucose homeostasis in a sex and phase-dependent manner, despite no effects on body weight gain or food intake. Interestingly, liver PEPCK expression was remarkably impacted by LEAP2 injections. The observed results suggests that perinatal LEAP2 exposure can modulate liver metabolism and systemic glucose homeostasis. In addition, these results, although not expressive, may just be the beginning of the metabolic imbalance that will occur in adulthood.
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