Abstract

Maternal obesity greatly affects next generations, elevating obesity risk in the offspring through perinatal programming and flawed maternal and newborn nutrition. The exact underlying mechanisms are poorly understood. Interleukin-6 (IL-6) mediates its effects through a membrane-bound receptor or by trans-signaling (tS), which can be inhibited by the soluble form of the co-receptor gp130 (sgp130). As IL-6 tS mediates western-style diet (WSD) effects via chronic low-grade inflammation (LGI) and LGI is an important mediator in brain–adipose tissue communication, this study aims at determining the effects of maternal obesity in a transgenic mouse model of brain-restricted IL-6tS inhibition (GFAPsgp130) on offspring’s short- and long-term body composition and epigonadal white adipose tissue (egWAT) metabolism. Female wild type (WT) or transgenic mice were fed either standard diet (SD) or WSD pregestationally, during gestation, and lactation. Male offspring received SD from postnatal day (P)21 to P56 and were metabolically challenged with WSD from P56 to P120. At P21, offspring from WT and transgenic dams that were fed WSD displayed increased body weight and egWAT mass, while glucose tolerance testing showed the strongest impairment in GFAPsgp130WSD offspring. Simultaneously, egWAT proteome reveals a characteristic egWAT expression pattern in offspring as a result of maternal conditions. IL-6tS inhibition in transgenic mice was in tendency associated with lower body weight in dams on SD and their respective offspring but blunted by the WSD. In conclusion, maternal nutrition affects offspring’s body weight and egWAT metabolism predominantly independent of IL-6tS inhibition, emphasizing the importance of maternal and newborn nutrition for long-term offspring health.

Highlights

  • Maternal obesity is a substantial problem as it does affect the mother’s wellbeing, but it increases the risk for birth complications and health problems in their children and, generations to come [1,2]

  • In order to assess maternal weight gain and development of glucose intolerance, all dams underwent weekly weighing from weaning until mating and every other day from mating until birth (Figure 1a)

  • IL-6tS inhibition can partially prevent detrimental effects of maternal western-style diet (WSD) feeding on offspring

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Summary

Introduction

Maternal obesity is a substantial problem as it does affect the mother’s wellbeing, but it increases the risk for birth complications and health problems in their children and, generations to come [1,2]. Poor maternal nutritional conditions during fetal development and early life induce both short-term and long-term adverse metabolic effects in the offspring associated with an increased risk of obesity and type 2 diabetes (T2D). Newborn nutrition is crucially influenced by maternal nutritional status starting from pregnancy and lactation in modulating fetal, neonatal, and infant growth. This concept is described as perinatal programming [3,4]. In order to understand the underlying mechanism of perinatal programming, shedding light on the organs involved in and affected by maternal obesity during critical periods is vital. An excess of visceral or epigonadal (eg) white adipose tissue (WAT) is linked to systemic low-grade inflammation (LGI), and WAT has been discovered as a very active, endocrine organ part-taking in the changes in metabolism seen in obese individuals [6]

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