Effect of Rourea coccinea on ethanol-induced male infertility in Wistar albino rats.

Ethanol consumption is a risk factor of male infertility. The use of medicinal plants offers an alternative for the treatment of male infertility in developing countries. This study aimed to evaluate the Rourea coccinea effect on ethanol-induced male infertility in Wistar rats. Twenty-five (25) male Wistar rats were randomised into five groups of five rats and treated by oesophageal gavage over a 28-day period. Group 1 (negative control) received distilled water; Group 2 (positive control) received 30% ethanol at 7 mg/kg body weight; Group 3 (reference control) received 30% ethanol co-treated with the reference drug, clomiphene citrate; Groups 4 and 5 (test groups) received 30% ethanol co-treated with Rourea coccinea hydro-ethanolic extract at 200 and 400 mg/kg respectively. Testosterone hormone, sperm parameters and testicular histopathology were evaluated. Ethanol treatment induced a significant reduction (p < .05) in sperm count, motility, viability and a significant increase in sperm abnormalities because of the significant decrease (p < .05) in testosterone levels. These data correlate with the alterations observed in the seminiferous tubule on histopathological examination of the testes. However, co-treatment of ethanol with Rourea coccinea extract or the reference drug restored the ethanol-induced toxic effects on the reproductive organs, sperm profile and testosterone level.

Peroxisome proliferator-activated receptor-alpha modulates insulin gene transcription factors and inflammation in adipose tissues in mice.

We have recently reported that PPAR alpha deficiency leads to hypoglycaemia and hypoinsulinemia in mice (Yessoufou et al. Endocrinology 147:4410-4418, 2006). Besides, these mice exhibited high adiposity with an inflammatory state. We, therefore, assessed, in this study, the effects of PPAR alpha deficiency on the expression of mRNA encoding for the insulin gene transcription factors in pancreatic beta-cells along with those implicated in inflammation in adipose tissues. On fasting, the adult PPAR alpha-null mice were hypoglycemic. Serum insulin concentrations and its pancreatic mRNA transcripts were downregulated in PPAR alpha-null mice, suggesting that PPAR alpha gene deletion contributes to low insulin gene transcription. The PPAR alpha gene deletion downregulates the mRNA expression of insulin gene transcription factors, i.e., Pdx-1, Nkx6.1, and MafA. Besides, the pancreatic function was diminished by PPAR alpha deficiency as PPAR alpha-null mice expressed low pancreatic Glut2 and glucokinase mRNA. PPAR alpha-null mice also expressed high adiponectin and leptin mRNA levels compared to wild type animals. Adipose tissues of PPAR alpha-null mice exhibited upregulation of CD14 and CD68 mRNA, generally expressed by macrophages. PPAR alpha gene deletion downregulates the adipocyte mRNA of certain pro-inflammatory agents, like MCP-1, TNF-alpha, IL-1 beta, IL-6, and RANTES, though pro-inflammatory TLR-2 and TLR-4 mRNAs were upregulated in the adipose tissues. Our results suggest that PPAR alpha deficiency, in mice, is implicated in the modulation of insulin gene transcription and inflammatory status in adipose tissues.

Antioxidant status and circulating lipids are altered in human gestational diabetes and macrosomia.

Fetuses from mothers with gestational diabetes are at increased risk of developing neonatal macrosomia and oxidative stress. We investigated the modulation of antioxidant status and circulating lipids in gestational diabetic mothers and their macrosomic babies and in healthy age-matched pregnant women and their newborns. The serum antioxidant status was assessed by employing anti-radical resistance kit (KRL; Kirial International SA, Couternon, France) and determining levels of vitamin A, C, and E and the activity of superoxide dismutase (SOD). Circulating serum lipids were quantified, and lipid peroxidation was measured as the concentrations of serum thiobarbituric acid-reactive substances (TBARS). As compared with non-diabetic mothers, gestational diabetic women exhibited decreased levels of vitamin E and enhanced concentrations of vitamin C without any changes in vitamin A. Vitamin A and C levels did not change in macrosomic babies except vitamin E whose levels were lower in these infants than in the newborns of non-diabetic mothers. Gestational diabetes mellitus (GDM) and macrosomia were also associated with impaired SOD activities and enhanced TBARS levels. Globally, total serum antioxidant defense status in diabetic mothers and their macrosomic babies was diminished as compared with control subjects. Triglyceride and cholesterol concentrations did not differ significantly between gestational diabetic and control mothers; however, macrosomia was associated with enhanced plasma cholesterol and triglyceride levels. These results suggest that human GDM and macrosomia are associated with downregulation of antioxidant status, and macrosomic infants also exhibit altered lipid metabolism.

Cassava-enriched diet is not diabetogenic rather it aggravates diabetes in rats.

Chronic intake of cassava has been thought to play a role in the pathogenesis of diabetes. We investigated the effects of dietary cassava (Manihot esculenta), which naturally contains cyanogenic glycosides, in the progression of diabetes mellitus in rats. Diabetes was induced by five mild doses of streptozotocin, in male Wistar rats which were fed a standard or cyanide-free cassava (CFC) diet containing or not containing exogenous cyanide with or without methionine. Methionine was employed to counterbalance the toxic effects of cyanide. During diabetes progression, we determined glycaemia and antioxidant status, by measuring vitamin C levels and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-Red). Feeding CFC diet did not induce diabetes in control rats; rather this diet, in diabetic animals, aggravated hyperglycaemia the severity of which was increased in these animals fed CFC diet, supplemented with cyanide. Addition of methionine curtailed the toxic effects of cyanide supplementation in CFC diet-fed diabetic animals. In standard diet-fed animals, the activities of SOD, GSH-Px and GSSG-Red were lower in diabetic rats than control rats. Interestingly, all of the CFC diets with or without cyanide or methionine, increased vitamin C levels and antioxidant enzyme activities in both control and diabetic animals. However, supplementing cyanide to CFC diet (without methionine) curtailed SOD and GSH-Px activities in diabetic rats. Our study shows that cassava diet containing cyanide is 'diabetes-aggravating'.