Forced catch-up growth after fetal protein restriction alters the adipose tissue gene expression program leading to obesity in adult mice

May 22, 2009American journal of physiology. Regulatory, integrative and comparative physiology

Rapid growth after protein shortage before birth changes fat tissue genes and leads to obesity in adult mice

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Abstract

At 9 months, male mice with fetal protein restriction showed increased relative fat mass and metabolic changes.

Fetal protein restriction followed by postnatal catch-up growth may lead to obesity in mice.
Mice from low-protein diets exhibited hyperglycemia, hypercholesterolemia, and hyperleptinemia at 9 months.
Alterations in adipose tissue gene expression were linked to the maternal diet during gestation.
Several genes involved in lipid metabolism showed changes in expression due to early nutrition mismatch.
Early mismatched nutrition could increase susceptibility to overweight when exposed to a high-calorie diet post-weaning.

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A mismatch between fetal and postnatal environment can permanently alter the body structure and physiology and therefore contribute later to obesity and related disorders, as revealed by epidemiological studies. Early programming of adipose tissue might be central in this observation. Moreover, adipose tissue secretes adipokines that provide a molecular link between obesity and its related disorders. Therefore, our aim was to investigate whether a protein restriction during fetal life, followed by catch-up growth could lead to obesity in 9-mo-old male mice and could alter the adipose tissue gene expression profile. Dams were fed a low-protein (LP) or an isocaloric control (C) diet during gestation. Postnatal catch-up growth was induced in LP offspring by feeding dams with control diet and by culling LP litters to four pups instead of eight in the C group. At weaning, male mice were fed by lab chow alone (C) or supplemented with a hypercaloric diet (HC), to induce obesity (C-C, C-HC, LP-C, and LP-HC groups). At 9 mo, LP offspring featured increased relative fat mass, hyperglycemia, hypercholesterolemia, and hyperleptinemia. Using a microarray designed to study the expression of 89 genes involved in adipose tissue differentiation/function, we demonstrated that the expression profile of several genes were dependent upon the maternal diet. Among the diverse genes showing altered expression, we could identify genes encoding several enzymes involved in lipid metabolism. These 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.

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Forced catch-up growth after fetal protein restriction alters the adipose tissue gene expression program leading to obesity in adult mice

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