Food sources for camptandriid crabs in an arid mangrove ecosystem of the Persian Gulf: a stable isotope approach.

Crabs of the family Camptandriidae are the most dominant burrowing crabs inhabiting arid mangrove forests of the Persian Gulf. They play important roles in the structuring and functioning of mangrove ecosystems by modulating biogeochemical processes and cycling of nutrients, serving as important ecosystem engineers. We analysed stable carbon (13C) and nitrogen (15N) isotope values of three camptandriid crabs (Opusia indica, Nasima dotilliformis, and Manningis arabicum) and their potential food sources in the Hara Biosphere Reserve, northern Persian Gulf. A Bayesian mixing model was used to estimate the contribution of potential food sources for consumers. The results showed that to some degree, all the four sources selected contributed to the camptandriid diets, but microphytobenthos made the most important contributions to the diet of the consumers. Mangroves do not appear to be a significant source of carbon in the diet of camptandriid crabs in the arid mangrove system of the Persian Gulf. Rather, they offer favourable growing conditions, thus boosting microphytobenthos production and availability for consumers which prefer a high nutritional and palatable source.

The Impact of Vitamin D Supplementation on Neurodegeneration, TNF-α Concentration in Hypothalamus, and CSF-to-Plasma Ratio of Insulin in High-Fat-Diet-Induced Obese Rats.

There is growing evidence that obesity can lead to neurodegeneration induced by pro-inflammatory cytokines such as tumor necrosis factor (TNF-α). Moreover, obesity is associated with reduced transport of insulin through the blood-brain barrier (BBB). Insulin deficiency in the brain especially in the hypothalamus region has neurodegenerative and obesity-promoting effects. Because of the anti-inflammatory and neuroprotective effects of vitamin D, in the current experimental study, we aimed to investigate the effects of vitamin D supplementation on neurodegeneration, TNF-α concentration in the hypothalamus, and cerebrospinal fluid (CSF) to serum ratio of insulin in high-fat-diet-induced obese rats. At the first phase of the study, the rats were divided into two groups: (1) normal diet (ND, 10% fat) and (2) high-fat diet (HFD, 59% fat) and were fed for 16 weeks. In the second phase, each group was subdivided into four groups including the following: ND, normal diet + vitamin D, HFD, and HFD + vitamin D. Weight was measured and recorded weekly. Vitamin D supplementation for 5 weeks at 500 IU/kg dosage was used. One week after vitamin D supplementation, daily food intake was recorded. At week 22, blood was collected to determine fasting serum glucose, vitamin D, and insulin concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. CSF samples were also collected to measure insulin concentrations, and the hypothalamus was dissected to determine TNF-α concentration. HFD significantly increased TNF-α concentrations and degenerated neurons in the hypothalamus (P = 0.02). We also observed a significant reduction of CSF-to-serum ratio of insulin in HFD group (P = 0.03). The HOMA-IR test indicated significant increment of insulin resistance in HFD-fed rats (P = 0.006). Vitamin D supplementation in HFD group significantly reduced weight (P = 0.001) and food intake (P = 0.008) and increased CSF-to-serum ratio of insulin (P = 0.01). Furthermore, vitamin D decreased insulin resistance in the HFD group (P = 0.008). Vitamin D had no significant effect on degenerated neurons and TNF-α concentration in the hypothalamus. According to our findings, vitamin D improved brain insulin homeostasis and modulated food intake and body weight in high-fat-diet-induced obese rats. Further studies are needed to better clarify the underlying mechanisms.

Protective role of lipoic acid on methotrexate induced intestinal damage in rabbit model.

Methotrexate (MTX), a folate antagonist agent, is mainly used in treatment of malignant tumors and auto immune diseases and affects not only tumor cells, but also gastrointestinal mucosa. The present study was undertaken to determine whether lipoic acid (LA) could ameliorate methotrexate-induced oxidative intestine injury in rabbits. Twenty-one rabbits were randomly assigned into three groups: Group 1 (control group), Group 2 (received 20 mg/kg MTX), Group 3 (received MTX plus LA 75 mg/kg orally). On the 6th day rabbits were anesthetized and intestinal tissue sampled for pathologic and biochemical assessment. The intestinal tissue injury index and malondialdehyde (MDA) levels were lower in MTX+LA group as compared to the MTX group, and tissue glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity were higher in MTX+LA group than in the MTX group (p < 0.05). These findings suggest that co-administration of LA with MTX is associated with reduction in oxidative injury and tissue damage in the intestine. We suggest that lipoic acid may have a protective role in the MTX-induced oxidative injury.