Abstract

The regulation of fetal development by bioactive substances such as hormones and neuropeptides derived from the gestational mother is considered to be essential for the development of the fetus. On the other hand, it has been suggested that changes in the physiological state of the pregnant mother due to various factors may alter the secretion of these bioactive substances and induce metabolic changes in the offspring, such as obesity, overeating, and inflammation, thereby affecting postnatal growth and health. However, our knowledge of how gestational maternal bioactive substances modulate offspring physiology remains fragmented and lacks a systematic understanding. In this mini-review, we focus on ghrelin, which regulates growth and energy metabolism, to advance our understanding of the mechanisms by which maternally derived ghrelin regulates the growth and health of the offspring. Understanding the regulation of offspring growth by maternally-derived ghrelin is expected to clarify the fetal onset of metabolic abnormalities and lead to a better understanding of lifelong health in the next generation of offspring.

Highlights

  • Ghrelin is a peptide hormone purified from the stomach as an endogenous ligand for the growth hormone (GH) secretagogue receptor (GHS-R) [1]

  • When ghrelin is administered continuously to a rat model of chronic heart failure, improvements in cardiac function are observed, including a decrease in peripheral vascular resistance, an increase in cardiac output, an increase in left ventricular ejection fraction, inhibition of left ventricular remodeling development, and promotion of compensatory cardiac hypertrophy in the non-infarcted area [14]. This is thought to be a direct effect of ghrelin and an effect mediated by GH/insulin-like growth factor-1 (IGF-1), which is increased by ghrelin [14]

  • This study found that chronic treatment of rat mothers with ghrelin increased birth weight, and that restricting maternal food intake with paired feeding after ghrelin administration stimulated fetal growth, while active maternal immunization decreased fetal weight during pregnancy [16]

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Summary

INTRODUCTION

Ghrelin is a peptide hormone purified from the stomach as an endogenous ligand for the GH secretagogue receptor (GHS-R) [1]. Plasma ghrelin concentration is inversely correlated with body mass index (BMI), and is reported to be low in obese individuals and high in cases of anorexia nervosa, severe heart failure, and lung cancer with strong cachexia This suggests that ghrelin is activated during negative energy balance and maintains homeostasis by stimulating food intake, fat accumulation, and lowering body temperature. When ghrelin is administered continuously to a rat model of chronic heart failure, improvements in cardiac function are observed, including a decrease in peripheral vascular resistance, an increase in cardiac output, an increase in left ventricular ejection fraction, inhibition of left ventricular remodeling development, and promotion of compensatory cardiac hypertrophy in the non-infarcted area [14] This is thought to be a direct effect of ghrelin and an effect mediated by GH/insulin-like growth factor-1 (IGF-1), which is increased by ghrelin [14].

Detection Methods References
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