Abstract
Impaired early nutrition influences the risk of developing metabolic disorders in later life. We observed that transient postnatal overfeeding (OF) in mice induces long-term hepatic alterations, characterized by microsteatosis, fibrosis associated with oxidative stress (OS), and stress-induced premature senescence (SIPS). In this study, we investigated whether such changes can be reversed by moderate calorie restriction (CR). C57BL/6 male mice pups were maintained during lactation in litters adjusted to nine pups in the normal feeding (NF) group and three pups in the transient postnatal OF group. At six months of age, adult mice from the NF and OF groups were randomly assigned to an ad libitum diet or CR (daily energy supply reduced by 20%) for one month. In each group, at the age of seven months, analysis of liver structure, liver markers of OS (superoxide anion, antioxidant defenses), and SIPS (lipofuscin, p53, p21, p16, pRb/Rb, Acp53, sirtuin-1) were performed. CR in the OF group reduced microsteatosis, decreased levels of superoxide anion, and increased protein expression of catalase and superoxide dismutase. Moreover, CR decreased lipofuscin staining, p21, p53, Acp53, and p16 but increased pRb/Rb and sirtuin-1 protein expression. CR did not affect the NF group. These results suggest that CR reduces hepatic disorders induced by OF.
Highlights
In recent years, the prevalence of obesity has dramatically increased worldwide and is considered a major global health problem
We explored whether moderate calorie restriction (CR) (20%) over a short period in adulthood can prevent hepatic structure alterations, liver oxidative stress (OS), and stress-induced premature senescence (SIPS) induced by transient postnatal OF in a mouse model
With Masson’s Trichrome staining, we observed that the mean percentage of hepatic fibrotic area was not significantly different between the livers from the overfeeding calorie restriction (OFCR) group and the livers from the OF
Summary
The prevalence of obesity has dramatically increased worldwide and is considered a major global health problem. In 40 years, the number of school-age children and adolescents with obesity has greatly increased from 11 million to 124 million [1]. Adverse health consequences of obesity are observed in many western populations and include higher blood pressure, obesity, glucose intolerance, dyslipidemia, decreased insulin sensitivity, and type 2 diabetes, which are components of metabolic syndrome (MetS) [2]. Nonalcoholic fatty liver disease (NAFLD), which is the major prevalent acquired chronic liver disease. Nutrients 2019, 11, 2796 in developed countries [3], is considered a hepatic manifestation of MetS [4]. Impaired nutritional conditions during early development, such as maternal and paternal undernutrition or overnutrition, maternal dietary imbalance during pregnancy, and altered early postnatal nutrition, are associated with the developmental programming of cardiometabolic diseases in adulthood [2]
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