title: Mechanical-tactile stimulation (MTS) intervention in a neonatal stress model alters adult adipose tissue deposition and prevents hyperinsulinemia in male rats.
abstract: Preterm infants are exposed to numerous stressors during hospitalization and by term corrected gestational age they have lower body weight but a greater proportion of total body as well as abdominal visceral adipose tissue (VAT) accumulation. Greater abdominal VAT stores have a known association with metabolic syndrome. Mechanical-tactile stimulation (MTS) improves modulation of stress response in both humans and rodents. We hypothesize that MTS, administered during an established model of neonatal stress, would decrease stress-driven adiposity and prevent associated metabolic imbalances in adult rats. Neonatal stress, administered to rat pups from postnatal days 5 to P9, consisted of needle puncture and hypoxic/hyperoxic challenge during 60 min of maternal separation (STRESS; n=20). Mechanical-tactile stimulation (MTS; n=20) was administered to rat pups for 10 min during maternal separation in the stress protocol. Control animals received standard care (CTL; n=20). MRI measured adult (P120) abdominal total fat mass, subcutaneous (SAT) and visceral adipose tissue (VAT). Body weight and fasting serum adiponectin, leptin, glucose, insulin, and corticosterone were also measured. STRESS results in elevated VAT/SAT ratio compared to CTL but lower abdominal total fat mass and abdominal SAT. STRESS males experience hyperinsulinemia. Both STRESS and MTS had elevated leptin with lower adiponectin and corticosterone compared to CTL. In summary, neonatal stress promotes greater abdominal VAT accumulation and, in males, caused hyperinsulinemia and hypoadiponectinemia. Importantly, MTS normalized the VAT/SAT ratio and prevented hyperinsulinemia. We speculate that MTS ameliorates some of the negative metabolic consequences of early life perturbations due to neonatal stress exposure.
authors.affiliation: Center for Pediatric Nutrition Research, University of Utah, Salt Lake City, Utah 84108, USA. shannon.haley@hsc.utah.edu
authors.forename: Shannon
authors.initials: S
authors.lastname: Haley
authors.forename: Kimberly
authors.initials: K
authors.lastname: Neff
authors.forename: Kristina
authors.initials: K
authors.lastname: Gulliver
authors.forename: Grace
authors.initials: G
authors.lastname: Gough
authors.forename: Hillarie
authors.initials: H
authors.lastname: Slater
authors.forename: Robert H
authors.initials: RH
authors.lastname: Lane
authors.forename: Laurie J
authors.initials: LJ
authors.lastname: Moyer-Mileur
mesh_terms: D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000503:physiopathology; D050154:Adiposity; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D001786:Blood Glucose; D003345:Corticosterone / Q000097:blood; D005260:Female; D006946:Hyperinsulinism / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D018496:Hyperoxia / Q000150:complications; D000860:Hypoxia / Q000150:complications; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D013312:Stress, Physiological; D013315:Stress, Psychological / Q000150:complications*; D014110:Touch
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D003345:Corticosterone