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Published on: March 12, 2019
Neonatal overfeeding causes higher adrenal catecholamine content and basal secretion and liver dysfunction in adult
E P S Conceição1, E G Moura, I H Trevenzoli
1Laboratory of Endocrine Physiology, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, RJ, Brazil.
Insights
Neonatal overfeeding in rats increases adrenal function and reduces liver beta-2 adrenergic receptors. This contributes to adult-onset hypertension and liver dysfunction, highlighting early-life nutrition
Area of Science:
- Endocrinology
- Metabolic Disorders
- Developmental Biology
Background:
- Neonatal overfeeding in rats leads to adult-onset hyperleptinemia, visceral adiposity, hypertension, and liver insulin resistance.
- Previous studies linked neonatal hyperleptinemia to adrenal medullary hyperfunction, hypertension, and liver steatosis in adulthood.
Purpose of the Study:
- To investigate alterations in adrenal and liver function in adult obese rats subjected to neonatal overfeeding.
- To determine if these functional changes underlie the observed hypertension and liver alterations.
Main Methods:
- Wistar rats were subjected to reduced litter size (3 pups/litter) from day 3 of lactation to weaning (SL group) to induce overfeeding.
- Control rats (NL group) had 10 pups per litter.
- Rats were maintained on a standard diet and water ad libitum until 180 days of age.
Main Results:
- SL rats showed increased adrenal catecholamine content and protein levels of tyrosine hydroxylase and DOPA decarboxylase, with higher basal catecholamine secretion.
- Hypothalamic-pituitary-adrenal cortex axis hormones remained unchanged.
- Liver beta-2 adrenergic receptor content was significantly reduced in SL rats (-45%), accompanied by increased liver glycogen and triglycerides, suggesting microsteatosis.
Conclusions:
- Neonatal overfeeding enhances adrenal medullary function but decreases hepatic beta-2 adrenergic receptor expression.
- These findings suggest a link between early-life overnutrition, altered adrenomedullary activity, and reduced hepatic beta-2 adrenergic signaling, contributing to obesity-related liver dysfunction and hypertension.
Purpose:
Rats that are overfed during lactation exhibit neonatal hyperleptinemia and higher visceral adiposity, hypertension, higher liver oxidative stress and insulin resistance in the liver as adults. Previously, we demonstrated that neonatal hyperleptinemia is associated with adrenal medullary hyperfunction, hypertension and liver steatosis in adulthood. Therefore, we hypothesised that adrenal and liver functions are altered in adult obese rats that were overfed during lactation, which would underlie their hypertension and liver alterations.
Methods:
The litter size was reduced from ten to three male pups on the third day of lactation until weaning (SL) to induce early overfeeding in Wistar rats. The control group had ten rats per litter (NL). Rats had free access to standard diet, and water after weaning until the rats were 180 days old.
Results:
The SL group exhibited higher adrenal catecholamine content (absolute: +35% and relative: +40%), tyrosine hydroxylase (+31%) and DOPA decarboxylase (+90%) protein contents and basal catecholamine secretion in vitro (+57%). However, the hormones of the hypothalamic-pituitary-adrenal cortex axis were unchanged. β₃-adrenergic receptor content in visceral adipose tissue was unchanged in SL rats, but the β₂-adrenergic receptor content in the liver was lower in this group (-45%). The SL group exhibited higher glycogen and triglycerides contents in the liver (+79 and +49%, respectively), which suggested microesteatosis.
Conclusions:
Neonatal overfeeding led to higher adrenomedullary function, but the liver β₂-adrenergic receptor content was reduced. These results may contribute to the hepatic dysfunction characteristic of liver obesity complications.
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