RESUMO

Vitamin D deficiency is common in pregnant women and infants. The present study aimed to investigate the effects of vitamin D restricted diet on the Wistar rats offspring penis morphology. Mother rats received either standard diet (SC) or vitamin D restricted (VitD) diet. At birth, offspring were divided into SC/SC (from SC mothers, fed with SC diet) and VitD/VitD (from VitD mothers, fed with VitD diet). After euthanasia the penises were processed for histomorphometric analysis. The VitD/VitD offspring displayed metabolic changes and reduction in the cross-sectional area of the penis, corpus cavernosum, tunica albuginea, and increased area of the corpus spongiosum. The connective tissue, smooth muscle, and cell proliferation percentages were greater in the corpus cavernosum and corpus spongiosum in the VitD/VitD offspring. The percentages of sinusoidal spaces and elastic fibers in the corpus cavernosum decreased. The elastic fibers in the tunica albuginea of the corpus spongiosum in the VitD/VitD offspring were reduced. Vitamin D restriction during perinatal and postnatal periods induced metabolic and structural changes and represented important risk factors for erectile dysfunction in the penis of the adult offspring. These findings suggest that vitamin D is an important micronutrient in maintaining the cytoarchitecture of the penis.

Assuntos

Pênis , Complicações na Gravidez , Deficiência de Vitamina D , Vitamina D , Animais , Feminino , Masculino , Pênis/citologia , Pênis/efeitos dos fármacos , Pênis/crescimento & desenvolvimento , Gravidez , Ratos , Ratos Wistar , Vitamina D/administração & dosagem , Vitamina D/sangue , Vitamina D/farmacologia

RESUMO

High-sucrose and high-fat diets induce deregulation in the metabolism of lipids and carbohydrates. This study aimed to detect the initial consequences on lipogenesis, gluconeogenesis and insulin signaling in the livers of rodents fed high-fat and/or high-sucrose diets for a short period of time. Male mice received a standard chow (SC), high-fat (HF), high-sucrose (HSu) or high-fat, high-sucrose (HFHSu) diet for 4 weeks. At euthanasia, blood was collected and the liver was removed for histomorphometrical and molecular analysis. The HF, HSu and HFHSu groups presented glucose intolerance, hepatomegaly, liver steatosis and lipid profile alteration when compared to the SC group (p < 0.0005). Additionally, there was an elevation in protein levels involved in lipogenesis (SREBP-1c), gluconeogenesis (PEPCK and G6Pase) and insulin signaling (IRS-1 and Akt) in the livers from the experimental groups compared to the SC group (p < 0.0005). Thus, we conclude that a short-term HF and/or HSu diet promotes glucose intolerance and liver damage in adult male mice. Surprisingly, the short exposure to excess sucrose in the diet promoted glucose intolerance and liver damage even in the absence of an increase in body mass or changes in serum insulin, cholesterol and triacylglycerol levels.