High-sucrose diet potentiates hyperaldosteronism and renal injury induced by stress in young adult rats.

Analyze the effect of stress and high-sucrose diet on serum aldosterone levels and the morphometric characteristics of the kidney in young adult rats. Wistar male rats aged 21 days old weaned were randomly assigned into four groups: control (C), stressed (St), high-sucrose diet (S30), and chronic restraint stress plus a 30% sucrose diet (St + S30). Rats were fed with a standard chow and tap water ad libitum (C group) or 30% sucrose diluted in water (S30 group) during eight weeks. The St and St + S30 groups were subject to restraint stress (1-hour daily in a plastic cylinder, 5 days per week), four weeks before euthanasia. At 81 days old, all animals were killed and blood samples and kidneys were collected. Stressed rats had an increase in the serum aldosterone and renal triacylglycerol, a decrease in the area of the renal corpuscle, glomeruli, proximal tubules, and aquaporin 2 expressions with loss of glomeruli. For its part, the high-sucrose diet decreased the area of the renal corpuscle, glomeruli, and aquaporin 2 expressions in the cortex. The combination of stress and high- sucrose diet maintained similar effects on the kidney as the stress alone, although it induced an increase in the creatinine levels and renal glycogen. Our results showed that chronic stress induces hyperaldosteronism and kidney injury. The intake of a high-sucrose diet may potentiate the renal injury promoted by stress.

Dietary intervention in adult rats exposed to a high-sugar diet early in life permanently impairs sperm quality.

Childhood obesity predicts the presence of adult obesity. Obesity is associated with poor sperm quality. We hypothesized that exposure to a high-sugar diet (HSD) in early life would cause permanent histomorphology damage to the testes, resulting in reduced sperm quality in adult life. Wistar rats (aged 21days) were divided into four groups (n=6). In the first experiment, the rats received tap water (control) and a 30% sucrose diet for two months (S30). In the second experiment, the control and 30% sucrose diets were fed for two months, followed by replacement with tap water for two months (IS30). Eating and drinking were monitored. Animals were then euthanized, visceral and gonadal fat tissue and testes were collected, and epididymal spermatozoa were excised. Testicular samples were used for morphological description by H&E staining and for quantifying triacylglycerol content, caspase activity, and oxidative stress. Serum testosterone concentration was evaluated. Spermatozoa were used to assess sperm quality. Our results show that sperm quality was impaired by consuming HSD and could not be restored by dietary intervention. HSD feeding induced hyperplasia of visceral adipose tissue, increased testicular weight, and serum testosterone levels. The dietary intervention increased visceral adipose tissue, serum, and testicular triacylglycerol levels and normalized serum testosterone levels. Overall, the HSD diet caused permanent changes in seminiferous tubule cross-sectional area, caspase activity, oxidative stress, and sperm quality. Therefore, a high-sugar diet in early life causes permanent damage to sperm quality in adulthood.

Kidney Adaptations Prevent Loss of Trace Elements in Wistar Rats with Early Metabolic Syndrome.

Metabolic syndrome (MetS) represents a cluster of related metabolic abnormalities, including central obesity, hypertension, dyslipidemia, hyperglycemia, and insulin resistance. These metabolic derangements present significant risk factors for chronic kidney disease that carries to loss of essential micronutrients, which accelerates comorbidity apparition. The work aimed was to evaluate the trace element homeostasis regarding morphological adaptations and renal function in MetS early-onset. Fifty male Wistar rats were divided into two groups: (a) control group and (b) hypercaloric diet group that developed MetS early-onset after 3 months. Classical zoometric parameters do not show changes; however, biochemical modifications were observed such as hyperglycemia, protein glycation, insulin resistance, dyslipidemia, hyperinsulinemia, and hypoadiponectinemia. MetS early-onset group observed renal structural modifications, but no functional changes. The structural modifications observed were minimal glomerular injury, glomerular basement membrane thickening, as well as mesangial and tubular cells that showed growth and proliferation. In serum and kidney (cortex and medulla), the concentrations of Zn, Fe, Cr, Mg, Mn, Cu, Co, and Ni were no differences between the experimental groups, but excretory fractions of these were lower in the hypercaloric diet group. In conclusion, MetS early-onset coexist renal structural modification and a hyperreabsorptive activity of essential trace elements that avoid its loss; thus, the excretory fraction of oligo-elements could be used a biomarker of early renal injury caused by metabolic diseases in the clinical practice.

Morphometric changes and AQP2 expression in kidneys of young male rats exposed to chronic stress and a high-sucrose diet.

OBJECTIVE: Consumption of a cafeteria-like diet and chronic stress have a negative impact on kidney function and morphology in adult rats. However, the interaction between chronic restraint stress and high-sucrose diet on renal morphology in young rats is unknown. A high-sucrose diet does not modify serum glucose levels but reduces serum corticosterone levels in stressed young rats, in this way it is confusing a possible potentiate or protector effect of this diet on kidney damage induced by stress. METHODS: Wistar male rats at 4 weeks of age were randomly assigned into 4 groups: control (C), stressed (St), high-sucrose diet (S30), and chronic restraint stress plus a 30% sucrose diet (St + S30). Rats were fed with a standard chow and tap water (C group) or 30% sucrose diluted in water (S30 group). Chronic restraint stress consisted of 1-h daily placement into a plastic cylinder, 5 days per week, and for 4 weeks. RESULTS: Stressed rats exhibited a low number of corpuscles, glomeruli, high number of mesangial cells, major deposition of mesangial matrix and aquaporin-2 protein (AQP-2) expression, and low creatinine levels. Meanwhile, high-sucrose diet ameliorated AQP-2 expression and avoided the reduction of creatinine levels induced by chronic stress. The combination of stress and high-sucrose diet maintained similar effects on the kidney as stress alone, although it induced a greater reduction in the area of proximal tubules. CONCLUSIONS: Our results show that both chronic stress and a high-sucrose diet induce histological changes, but chronic stress may generate an accelerated glomerular hypertrophy associated with functional changes before puberty.