Neonatal nutritional programming induces gliosis and alters the expression of T-cell protein tyrosine phosphatase and connexins in male rats

Horm Behav. 2020 Apr:120:104690. doi: 10.1016/j.yhbeh.2020.104690. Epub 2020 Jan 23.

Abstract

Changes to neonatal nutrition result in long-lasting impairments in energy balance, which may be described as metabolic programing. Astrocytes, which are interconnected by gap junctions, have emerged as important players in the hypothalamic control of food intake. In order to study the effects of nutritional programming on glial morphology and protein expression, cross-fostered male Wistar rats at postnatal day 3 were assigned to three groups based on litter size: small litter (3 pups per dam, SL), normal litter (10 pups per dam, NL), and large litter (16 pups per dam, LL). Rats from the SL group exhibited higher body weight throughout the study and hyperphagia after weaning. LL animals exhibited hyperphagia, high energy efficiency and catch-up of body weight after weaning. Both the SL and LL groups at postnatal day 60 (PN60) exhibited increased levels of plasma leptin, the Lee index (as an index of obesity), adiposity content, immunoreactivity toward T-cell protein tyrosine phosphatase (TCPTP), and glial fibrillary acidic protein (GFAP) in the arcuate nucleus (ARC) of the hypothalamus. Astrocyte morphology was altered in the ARC of SL and LL animals, and this effect occurred in parallel with a reduction in immunoreactivity toward connexin 30 (CX30). The data obtained demonstrate that both neonatal over- and underfeeding promote not only alterations in the metabolic status but also morphological changes in glial cells in parallel with increasing TCPTP and changes in connexin expression.

Keywords: CX30; CX43; Glia; Hypothalamus; Nutritional programming; TCPTP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiposity / physiology
  • Animal Nutritional Physiological Phenomena*
  • Animals
  • Animals, Newborn
  • Connexins / genetics*
  • Connexins / metabolism
  • Female
  • Gene Expression Regulation, Developmental
  • Gliosis / etiology*
  • Gliosis / genetics
  • Gliosis / metabolism
  • Hyperphagia / complications
  • Hyperphagia / genetics
  • Hyperphagia / metabolism
  • Hyperphagia / pathology
  • Hypothalamus / metabolism
  • Litter Size / physiology
  • Male
  • Obesity / complications
  • Obesity / genetics
  • Obesity / metabolism
  • Obesity / pathology
  • Pregnancy
  • Protein Tyrosine Phosphatase, Non-Receptor Type 2 / genetics*
  • Protein Tyrosine Phosphatase, Non-Receptor Type 2 / metabolism
  • Rats
  • Rats, Wistar
  • Sex Factors
  • Time Factors

Substances

  • Connexins
  • Protein Tyrosine Phosphatase, Non-Receptor Type 2