Myo-Inositol Supplementation in Suckling Rats Protects against Adverse Programming Outcomes on Hypothalamic Structure Caused by Mild Gestational Calorie Restriction, Partially Comparable to Leptin Effects.

Pedro Castillo,Catalina Picó,Mariona Palou,Zhi Xin Yau-Qiu,Andreu Palou,Ana M Rodríguez

doi:10.3390/nu13093257

Pedro Castillo, Catalina Picó + Show 4 more

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https://doi.org/10.3390/nu13093257

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Journal: Nutrients	Publication Date: Sep 18, 2021
Citations: 5	License type: CC BY 4.0

Affiliation: Universitat de les Illes Balears

Abstract

We studied whether myo-inositol supplementation throughout lactation, alone and combined with leptin, may reverse detrimental effects on hypothalamic structure and function caused by gestational calorie gestation (CR) in rats. Candidate early transcript-based biomarkers of metabolic health in peripheral blood mononuclear cells (PBMC) were also studied. Offspring of dams exposed to 25% gestational CR and supplemented during lactation with physiological doses of leptin (CR-L), myo-inositol (CR-M), the combination (CR-LM), or the vehicle (CR-V) as well as control rats (CON-V) were followed and sacrificed at postnatal day 25. Myo-inositol and the combination increased the number of neurons in arcuate nucleus (ARC) (only in females) and paraventricular nucleus, and myo-inositol (alone) restored the number of αMSH+ neurons in ARC. Hypothalamic mRNA levels of Lepr in CR-M and Insr in CR-M and CR-LM males were higher than in CR-V and CON-V, respectively. In PBMC, increased expression levels of Lrp11 and Gls in CR-V were partially normalized in all supplemented groups (but only in males for Gls). Therefore, myo-inositol supplementation throughout lactation, alone and combined with leptin, reverts programmed alterations by fetal undernutrition on hypothalamic structure and gene expression of potential early biomarkers of metabolic health in PBMC, which might be attributed, in part, to increased leptin sensitivity.

Highlights

Gestation and lactation are critical developmental windows in the programming of later metabolic health [1,2]
This parameter was normalized to that of control in animals treated with leptin or myo-inositol but not in those treated with the combination
Cumulative food intake from postnatal day 21 to 25 was lower in CR rats compared to controls and partially normalized in animals supplemented with myo-inositol but not in those treated with leptin or the combination

Summary

Introduction

Gestation and lactation are critical developmental windows in the programming of later metabolic health [1,2]. Both epidemiological evidences and animal studies have shown that adverse in-utero conditions can predispose the offspring to overweight/obesity and related metabolic alterations, such as insulin resistance, in adulthood [2,3,4,5]. Epidemiological studies have reported that breastfeeding compared to infant formula feeding provides numerous benefits to offspring health in the short term and in the longer term, exerting a protection against the development of obesity and other associated disorders in adulthood [10,11,12]. The specific mechanisms and factors that account for the benefits of breast milk are still uncertain, but specific milk compounds may play a role

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