Catch-up growth and obesity in male mice

  title={Catch-up growth and obesity in male mice},
  author={Susan E. Ozanne and Charles Nicholas Hales},
Poor fetal growth is linked with long-term detrimental effects on health in adulthood1. Here we investigate whether the lifespan of male mice is affected by their growth rate when they were suckling and find that limiting growth during that period not only increases longevity but also protects against the life-shortening effect of an obesity-inducing diet later on. By contrast, we find that lifespan is considerably shortened if the postnatal period of growth is accelerated to make up for… 
Poor fetal growth followed by rapid postnatal catch-up growth leads to premature death
Longevity is impacted by growth hormone action during early postnatal period
It is reported that GH treatment limited to a few weeks during development influences the lifespan of long-lived Ames dwarf and normal littermate control mice in a genotype and sex-specific manner, suggesting that developmental programming of aging importantly contributes to (and perhaps explains) the well documented developmental origins of adult disease.
Increased adiposity programmed by catch-up growth: requirement for leptin signals?
A report in this issue of Endocrinology is the first to examine whether leptin signals are required for programming of increased adiposity due to accelerated catch-up growth, and the role of neonatal leptin in mediating persistent effects of catch- up growth on metabolic phenotypes.
Neonatal Catch Up Growth Increases Diabetes Susceptibility But Improves Behavioral and Cardiovascular Outcomes of Low Birth Weight Male Mice
Two studies use isogenic mice with natural variation in perinatal growth to test the hypothesis that neonatal catch up growth improves the neurobehavioral and cardiovascular outcomes of low-birth weight mice, despite an increase in diabetes susceptibility and suggest an earlier window of vulnerability among growth restricted female mice.
Long-lived crowded-litter mice exhibit lasting effects on insulin sensitivity and energy homeostasis.
Glucose and insulin tolerance tests show an increase in insulin sensitivity in 6 mo old CL male mice, and females become more insulin sensitive later in life, which shows that early-life nutrient intervention has a significant lifelong effect on metabolic characteristics that may contribute to the increased lifespan of CL mice.
Nutritional limitation in early postnatal life and its effect on aging and longevity in rodents
Experimental evidence for long-term programming effects of early diet.
Global nutrient restriction confined to periods of early development programmes adult physiology in a manner that may predispose to later disease given the appropriate environmental stimuli is found.
Forced catch-up growth after fetal protein restriction alters the adipose tissue gene expression program leading to obesity in adult mice.
Results indicated that offspring submitted to early mismatched nutrition exhibited alterations in adipose tissue gene expression that probably increases their susceptibility to overweight when challenged after weaning with a HC diet.
Leptin-independent programming of adult body weight and adiposity in mice.
It is shown that low birth weight followed by rapid catch-up growth during lactation (recuperated offspring) leads to a persistent increase in body weight in adult life, both in wild-type and ob/ob animals.


Early protein restriction and obesity independently induce hypertension in 1-year-old rats.
The early 8% protein rats had significantly increased blood pressures, as did the cafeteria-fed rats, suggesting that early protein restriction, and later obesity, are indeed independent risk factors for the development of hypertension.
Longevity in obese and lean male and female rats of the Zucker strain: prevention of hyperphagia.
Zucker obese (fa/fa) and lean (Fa/Fa) rats were fed a soy protein diet ad libitum under barrier conditions from 4 wk of age until death. Obese rats were also pair fed with lean controls to prevent
The thrifty phenotype hypothesis.
It is proposed that the epidemiological associations between poor fetal and infant growth and the subsequent development of type 2 diabetes and the metabolic syndrome result from the effects of poor nutrition in early life, which produces permanent changes in glucose-insulin metabolism.
The Endocrine Regulation of Aging by Insulin-like Signals
Despite the similarities among mammals and invertebrates in insulin-like peptides and their signal cascade, more research is needed to determine whether these signals control aging in the same way in all the species by the same mechanism.
Historical claims and current interpretations of replicative aging
Experiments over the past several years have identified species in which replicative aging does not occur and many examples in which a failure to proliferate has been misinterpreted as replicative senescence, and insights from these studies now permit a reevaluation of much of the seemingly contradictory data concerning replicative Aging.