Evaluation of the anti-inflammatory and antioxidant effects of the microalgae Nannochloropsis gaditana in streptozotocin-induced diabetic rats.

PURPOSE: This study aims to evaluate the anti-inflammatory and antioxidant effects of N. gaditana on streptozotocin (STZ)-induced diabetes mellitus in Wistar rats. METHODS: Diabetes was induced in male Wistar rats by single intraperitoneal injection of STZ (45 mg/kg). Male rats were fed on control diet supplemented or not with N. gaditana (10%) for a period of 2 months. At the end of the experiment, biochemical parameters and oxidant/antioxidant markers in liver and pancreas tissues, as well as mitochondria isolated from liver of rats, were determined. RESULTS: It was notice that levels of glucose, glycated hemoglobin (HbA1c), lipid profile, kidney functions and liver enzymes in addition to markers of the inflammatory reactions interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) increased significantly (P < 0.05) in diabetic rats. Moreover, undesirable alterations of oxidative stress markers of tissue and mitochondria isolated from the liver were noted in these rats. N. gaditana supplementation was shown effective in lowering the levels of glucose, HbA1c and improving the renal and hepatic function and also in attenuating the oxidative stress and inflammation in diabetic rats. CONCLUSION: N. gaditana possesses antioxidant properties that might have beneficial effect in treatment of diabetes.

Effects of Highly-pure-enriched-cellulose Diet on Digestibility, Lipid Metabolism and Redox Status in Obese Offspring of Streptozotocin-Induced Diabetic Rats.

The long-term nutritional efficacy of a highly-pure-enriched-cellulose (HPEC) diet and its effects on lipid metabolism and oxidant/antioxidant status were investigated in obese offspring of streptozotocin-induced diabetic rats. Diabetes in pregnant rats was induced by intraperitoneal injection of streptozotocin on day 5 of gestation. Control pregnant rats were injected with citrate buffer. At weaning offspring of diabetic and control rats were fed HPEC or control diet, they were housed individually in metabolic cage for 2 months to investigate the nutritional efficacy of the diets. Consumption of HPEC diet decrease weight gain and energy intake, increase fecal weight and reduce lipid and protein digestibility; however, these diet had no effect on protein utilization, and nitrogen balance remained positive which confirms that HPEC diet had no significant long-term nutritional risks. Indeed for obese offspring from diabetic rats, these diet associated with high satiety promote weight loss, and provide reasonable glycemic control, these diet also lower blood lipids concentration and correct the imbalance of oxidant/antioxidant system. HPEC diet had a protective effect against long-term metabolic abnormalities associated with macrosomia.

Altered adipose tissue metabolism in offspring of dietary obese rat dams.

To investigate further the mechanisms of developmental programming, we analysed the effects of maternal overnutrition and of postnatal high-fat feeding on adipose tissue metabolism in the offspring. Postnatal changes in serum adiponectin, leptin and TAG [triacylglycerol (triglyceride)] levels, adipose tissue TAGs, fatty acids and enzyme activities were determined in offspring of cafeteria-diet-fed dams during gestation and lactation, weaned on to standard chow or on to cafeteria diet. Obese rats showed higher adiposity (+35% to 85%) as well as a significant increase in serum glucose, insulin, leptin, adiponectin and TAG levels (P<0.01) and adipose tissue LPL (lipoprotein lipase) and GPDH (glycerol-3-phosphate dehydrogenase) activities (P<0.01), compared with control pups at weaning (day 21) and at adulthood (day 90). Adipose HSL (hormone-sensitive lipase) activity was increased only at day 90 (P<0.05), and FAS (fatty acid synthase) activity remained unchanged. The proportions of SFAs (saturated fatty acids) and MUFAs (mono-unsaturated fatty acids) and the Δ(9)-desaturation index were significantly increased (P<0.05), whereas PUFAs (polyunsaturated fatty acids) were decreased (P<0.01) in serum and adipose TAGs of obese pups compared with controls. The cafeteria diet at weaning induced more severe abnormalities in obese rats. In conclusion, maternal overnutrition induced permanent changes in adipose tissue metabolism of the offspring. These pre-existing alterations in offspring were worsened under a high-fat diet from weaning to adulthood. Consequently, adipose adipokines and enzymes could provide a potential therapeutic target, and new investigations in this field could constitute strategies to improve the impact of early-life overnutrition.

Hepatic and very low-density lipoprotein fatty acids in obese offspring of overfed dams.

The combined effects of developmental programming and high-fat feeding at weaning on fatty acid metabolism of the offspring are not well known. In the present study, we aim at characterizing the influence of maternal and offspring's own diets on liver and very low-density lipoprotein (VLDL) lipids; fatty acid profiles of VLDL and liver phospholipids, triglycerides, and cholesteryl esters; and hepatic enzyme activities. Twenty obese male rats born to cafeteria diet-fed dams and 20 control rats born to control diet-fed dams were selected. At weaning, 10 rats of each group were fed control or cafeteria diet. Obese rats had a significant increase in serum glucose, insulin, leptin, VLDL apolipoprotein B100 and lipid levels, and hepatic fatty acid synthase and a reduction in acyl-coenzyme A oxidase and dehydrogenase activities compared with control pups at day 21 and day 90. Hepatic steatosis was apparent only at day 90. The proportions of saturated fatty acids and monounsaturated fatty acids and the oleic to stearic acid ratio were significantly increased, whereas polyunsaturated fatty acids and the arachidonic to linoleic acid ratio were decreased, in liver and VLDL lipids of obese pups compared with controls. The cafeteria diet at weaning induced more severe abnormalities in obese rats. In conclusion, maternal cafeteria diet induced a permanent reduction in hepatic ß-oxidation and an increase in hepatic lipogenesis that caused liver steatosis and VLDL and fatty acid alterations in adult offspring. These preexisting alterations in offspring were worsened under a high-fat diet from weaning to adulthood. Nutritional recommendations in obesity must then target maternal and postnatal nutrition, especially fatty acid composition.

Time course of changes in serum oxidant/antioxidant status in overfed obese rats and their offspring.

The aim of the present study was to determine the time course of changes in oxidant/antioxidant status, as well as serum glucose, insulin, leptin and lipid levels, liver adipose tissue and muscle lipid and protein contents, in cafeteria-diet-fed dams during gestation and lactation, and in their offspring throughout adulthood. Food intake was also evaluated. The cafeteria diet induced a significant increase in maternal body and relative adipose tissue weights, daily energy intake, and plasma glucose, insulin, leptin and lipid levels at parturition (day 0) and at the end of lactation (day 21). Plasma total antioxidant status [ORAC (oxygen radical absorbance capacity)], erythrocyte catalase and SOD (superoxide dismutase) activities were lower, whereas plasma hydroperoxide and carbonyl protein levels were higher in cafeteria-diet-fed mothers compared with control mothers at days 0 and 21. Pups from cafeteria-diet-fed dams, both males and females, also had consistently higher body and relative adipose tissue weights, and plasma glucose, insulin, leptin, triacylglycerol (triglyceride) and cholesterol levels at birth (day 0), weaning (day 21) and 3 months of age (day 90). These offspring had significantly lower ORAC and catalase activity, and higher plasma hydroperoxide and carbonyl protein levels and SOD activity at birth, at days 21 and 90 compared with control offspring. In conclusion, excessive maternal fat and energy intake can play an important role in the development of metabolic disorders in the offspring. Maternal oxidative stress may be among the responsible factors. Fetal oxidative stress may present an additional confounding influence and probably contributes to additional disorders, aggravating features of the metabolic syndrome. An improvement in maternal oxidant/antioxidant status during pregnancy and lactation, with adequate nutrition, could have beneficial effects on the progeny.