Prenatal hypoxia predisposes vascular functional and structural changes associated with oxidative stress damage and depressive behavior in adult offspring male rats.

Intrauterine hypoxia-ischemia (HI) provides a strong stimulus for a developmental origin of both the central nervous system and cardiovascular diseases. This study aimed to investigate vascular functional and structural changes, oxidative stress damage, and behavioral alterations in adult male offspring submitted to HI during pregnancy. The pregnant Wistar rats had a uterine artery clamped for 45 min on the 18th gestational day, submitting the offspring to hypoxic-ischemic conditions. The Sham group passed to the same surgical procedure as the HI rats, without occlusion of the maternal uterine artery, and the controls consisted of non-manipulated healthy animals. After weaning, the male pups were divided into three groups: control, sham, and HI, according to the maternal procedure. At postnatal day 90 (P90), the adult male offspring performed the open field and forced swim tests. In P119, the rats had their blood pressure checked and were euthanized. Prenatal HI induced a depressive behavior in adult male offspring associated with a reduced vasodilator response to acetylcholine in perfused mesenteric arterial bed, and reduced superoxide dismutase and glutathione peroxidase activities in the aorta compared to control and sham groups. Prenatal HI also increased the vasoconstrictor response to norepinephrine, the media thickness, collagen deposition, and the oxidative damage in the aorta from adult male offspring compared to control and sham groups. Our results suggest an association among prenatal HI and adult vascular structural and functional changes, oxidative stress damage, and depressive behavior.

Antidiabetic effect of Euterpe oleracea Mart. (açaí) extract and exercise training on high-fat diet and streptozotocin-induced diabetic rats: A positive interaction.

A growing body of evidence suggests a protective role of polyphenols and exercise training on the disorders of type 2 diabetes mellitus (T2DM). We aimed to assess the effect of the açaí seed extract (ASE) associated with exercise training on diabetic complications induced by high-fat (HF) diet plus streptozotocin (STZ) in rats. Type 2 diabetes was induced by feeding rats with HF diet (55% fat) for 5 weeks and a single dose of STZ (35 mg/kg i.p.). Control (C) and Diabetic (D) animals were subdivided into four groups each: Sedentary, Training, ASE Sedentary, and ASE Training. ASE (200 mg/kg/day) was administered by gavage and the exercise training was performed on a treadmill (30min/day; 5 days/week) for 4 weeks after the diabetes induction. In type 2 diabetic rats, the treatment with ASE reduced blood glucose, insulin resistance, leptin and IL-6 levels, lipid profile, and vascular dysfunction. ASE increased the expression of insulin signaling proteins in skeletal muscle and adipose tissue and plasma GLP-1 levels. ASE associated with exercise training potentiated the reduction of glycemia by decreasing TNF-α levels, increasing pAKT and adiponectin expressions in adipose tissue, and IR and pAMPK expressions in skeletal muscle of type 2 diabetic rats. In conclusion, ASE treatment has an antidiabetic effect in type 2 diabetic rats by activating the insulin-signaling pathway in muscle and adipose tissue, increasing GLP-1 levels, and an anti-inflammatory action. Exercise training potentiates the glucose-lowering effect of ASE by activating adiponectin-AMPK pathway and increasing IR expression.