scholarly journals Gestational Protein Restriction Increases Cardiac Connexin 43 mRNA levels in male adult rat offspring

Author(s):  
Kamila Fernanda Rossini ◽  
Camila Andrea de Oliveira ◽  
Hércules Jonas Rebelato ◽  
Marcelo Augusto Marreto Esquisatto ◽  
Rosana Catisti
2006 ◽  
Vol 100 (2) ◽  
pp. 642-648 ◽  
Author(s):  
Xing-Hai Yao ◽  
Li Chen ◽  
B. L. Grégoire Nyomba

Rat offspring exposed to ethanol (EtOH rats) during pregnancy are insulin resistant, but it is unknown whether they have increased gluconeogenesis. To address this issue, we determined blood glucose and liver gluconeogenic genes, proteins, and enzyme activities before and after insulin administration in juvenile and adult EtOH rats and submitted adult EtOH rats to a pyruvate challenge. In juvenile rats, basal glucose; peroxisome proliferator-activated receptor-coactivator-1α protein and mRNA; and phospho enolpyruvate carboxykinase enzyme activity, protein, and mRNA were similar between groups. After insulin injection, these parameters failed to decrease in EtOH rats, but glucose decreased by 30% and gluconeogenic enzymes, proteins, and mRNAs decreased by 50–70% in control rats. In adult offspring, basal peroxisome proliferator-activated receptor-coactivator-1α protein and mRNA levels were 40–80% higher in EtOH rats than in controls. Similarly, basal phospho enolpyruvate carboxykinase activity, protein, and mRNA were ∼1.8-fold greater in EtOH rats than in controls. These parameters decreased by ∼50% after insulin injection in control rats, but they remained unchanged in EtOH rats. After insulin injection in the adult rats, glucose decreased by 60% in controls but did not decrease significantly in EtOH rats. A subset of adult EtOH rats had fasting hyperglycemia and an exaggerated glycemic response to pyruvate compared with controls. The data indicate that, after prenatal EtOH exposure, the expression of gluconeogenic genes is exaggerated in adult rat offspring and is insulin resistant in both juvenile and adult rats, explaining increased gluconeogenesis. These alterations persist through adulthood and may contribute to the pathogenesis of Type 2 diabetes after exposure to EtOH in utero.


2014 ◽  
Vol 66 (9) ◽  
pp. 1328-1338 ◽  
Author(s):  
Graziele Freitas de Bem ◽  
Cristiane Aguiar da Costa ◽  
Paola Raquel Braz de Oliveira ◽  
Viviane Silva Cristino Cordeiro ◽  
Izabelle Barcellos Santos ◽  
...  

Biology Open ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. bio038562
Author(s):  
Bárbara Vaccari Cardoso ◽  
Augusto Henrique Custódio ◽  
Patrícia Aline Boer ◽  
José Antonio Rocha Gontijo

2006 ◽  
Vol 291 (3) ◽  
pp. R796-R802 ◽  
Author(s):  
Korami Dembele ◽  
Xing-Hai Yao ◽  
Li Chen ◽  
B. L. Grégoire Nyomba

Prenatal ethanol (EtOH) exposure is associated with low birth weight, followed by increased appetite, catch-up growth, insulin resistance, and impaired glucose tolerance in the rat offspring. Because EtOH can induce oxidative stress, which is a putative mechanism of insulin resistance, and because of the central role of the hypothalamus in the regulation of energy homeostasis and insulin action, we investigated whether prenatal EtOH exposure causes oxidative damage to the hypothalamus, which may alter its function. Female rats were given EtOH by gavage throughout pregnancy. At birth, their offspring were smaller than those of non-EtOH rats. Markers of oxidative stress and expression of neuropeptide Y and proopiomelanocortin (POMC) were determined in hypothalami of postnatal day 7 (PD7) and 3-mo-old (adult) rat offspring. In both PD7 and adult rats, prenatal EtOH exposure was associated with decreased levels of glutathione and increased expression of MnSOD. The concentrations of lipid peroxides and protein carbonyls were normal in PD7 EtOH-exposed offspring, but were increased in adult EtOH-exposed offspring. Both PD7 and adult EtOH-exposed offspring had normal neuropeptide Y and POMC mRNA levels, but the adult offspring had reduced POMC protein concentration. Thus only adult offspring preexposed to EtOH had increased hypothalamic tissue damage and decreased levels of POMC, which could impair melanocortin signaling. We conclude that prenatal EtOH exposure causes hypothalamic oxidative stress, which persists into adult life and alters melanocortin action during adulthood. These neuroendocrine alterations may explain weight gain and insulin resistance in rats exposed to EtOH early in life.


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