Overweight and metabolic and hormonal parameter disruption are induced in adult male mice by manipulations during lactation period.

Department of Drug Research and Evaluation, Istituto Superiore di Sanità, Roma, Italy.
Pediatric Research (Impact Factor: 2.84). 02/2006; 59(1):111-5. DOI: 10.1203/01.pdr.0000190575.12965.ce
Source: PubMed

ABSTRACT Neonatal manipulations (10 min of maternal separation plus s.c. sham injection, daily for the first 21 d of life) determine overweight in male adult mice. In this work, we investigated the mechanisms underlying mild obesity and the alteration of caloric balance. Neonatally manipulated mice become overweight after onset of maturity, showing increased fat tissue and hypertrophic epididymal adipocytes. Increase in body weight occurs in the presence of a small increase in daily food intake (significant only in the adult period) and the absence of a decrease in spontaneous locomotor activity, while the calculated caloric efficiency is higher in manipulated mice, especially in adulthood. Fasting adult animals show hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, and hyperleptinemia. Soon after weaning and in the adulthood, plasma corticosterone and adrenocorticotropin (ACTH) are also significantly increased. Thus, neonatal manipulations in nongenetically susceptible male mice program mild obesity, with metabolic and hormonal alterations that are similar to those found in experimental models of diabetes mellitus, suggesting that this metabolic derangement may have at least part of its roots early on in life and, more interestingly, that psychological and nociceptive stimuli induce these features.

  • Revista de Nutrição 01/2010; 23(1). DOI:10.1590/S1415-52732010000100010 · 0.35 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Summary We studied mechanisms contributing to stimulus-evoked changes in NAD(P)H fluorescence as a marker of neuronal activation in barrel cortex slices of the mouse. Electrical stimuli were set at frequency (50 Hz), which produced optimal responses and did not induce consistent bleaching of cells. With these stimuli, biphasic fluorescence changes were produced, which were composed of an initial transient decrease ("initial component", 1-3%), followed by a longer lasting transient increase ("overshoot", 1-8%). These responses, which were found to reflect mitochondrial function, were also used to test possible differences between brain function in adult control mice, and in adult mice which during lactation period underwent daily brief (10 min) mother deprivation plus sham injection. Preliminary results show that neonatally stressed adult mice have an initial component with similar amplitude, followed by a consistently higher overshoot. These results may be considered as a new and interesting direction among long-term or permanent changes induced by neonatal stress on brain structures.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic, epigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated early life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many maternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy (hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In neonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin resistance or T2DM. Unfavorable environments (socioeconomic situation and famine) or obesity also has long-term negative effects on children by causing increased susceptibility to T2DM in adults. We also address the potential mechanisms that may underlie the developmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving pre- and/or postnatal factors.
    Journal of Diabetes Research 12/2013; 2013:485082. DOI:10.1155/2013/485082 · 3.54 Impact Factor

Full-text (2 Sources)

Available from
Jun 10, 2014

Similar Publications