Increased cerebellar PET glucose metabolism corresponds to ataxia in Wernicke-Korsakoff syndrome

AIMS: To investigate a possible relationship between cerebellar glucose metabolism and recovery from ataxia in the first months of acute Wernicke-Korsakoff syndrome. METHODS: Two cases of alcoholic Wernicke-Korsakoff syndrome were followed up with the clinical status and cerebral glucose metabolism over a 4- and 9-month period. RESULTS: Initially both patients showed severe ataxia and elevated cerebellar glucose metabolism that decreased corresponding to the restitution of stance and gait. CONCLUSION: Increased cerebellar glucose metabolism at the onset of the illness may reflect the reorganization process of disturbed motor skills and may indicate cerebellar plasticity.     

Dietary antioxidants and glucose metabolism

PURPOSE OF REVIEW: Oxidative stress seems to play a pathogenic role in the vicious circle linking obesity, insulin resistance and type 2 diabetes. Hypothetically, dietary antioxidants should decrease oxidative stress and therefore improve glucose metabolism. However, many interventional trials evaluating the effect of antioxidant supplementation on insulin resistance, plasma glucose levels and risk of type 2 diabetes gave inconsistent results. RECENT FINDINGS: Many studies have recently demonstrated a positive effect of vitamin supplementation and of food enriched in antioxidant (seafood, whole nut, etc.) on markers of oxidative stress, insulin resistance, fasting plasma glucose and incidence of diabetes. The present paper critically reviews the consolidated notions on dietary antioxidant in view of the recent evidences. SUMMARY: Although a definitive estimation of the impact of dietary antioxidants on glucose metabolism is still lacking, food with high antioxidant concentrations seems to have a protective effect, improving oxidative stress-mediated detrimental effects on the vicious circle among obesity, insulin resistance and redox imbalance.     

Inhibitors of cannabinoid receptors and glucose metabolism

PURPOSE OF REVIEW: Abdominal obesity is closely related to type 2 diabetes and overactivity of the endocannabinoid system. The present review aims at evaluating the role of endocannabinoid system in glucose dysregulation and the effects of cannabinoid 1 receptor blockade on glucose metabolism in both animal models and overweight/obese humans, especially with type 2 diabetes. RECENT FINDINGS: Cannabinoid 1 receptors have been identified not only in the brain, but also in the adipose tissue, the gut, the liver, the skeletal muscle and even the pancreas, all organs playing a key role in glucose metabolism and type 2 diabetes. Rimonabant, the first selective cannabinoid 1 receptor blocker in clinical use, has been shown to reduce body weight, waist circumference, glycated haemoglobin, triglycerides, insulin resistance index, and to increase HDL cholesterol and adiponectin concentrations in patients with type 2 diabetes, confirming data on nondiabetic overweight/obese patients. Almost half of the metabolic changes, including glycated haemoglobin reduction, could not be explained by weight loss, in agreement with direct peripheral effects. SUMMARY: Cannabinoid 1 blockade reduces food intake and body weight and improves metabolic regulation beyond just weight loss. Because of its positive effect on glucose metabolism, rimonabant deserves consideration in the treatment of overweight/obese patients with type 2 diabetes.     

Increased 137Cs metabolism during pregnancy

A woman temporarily visiting the Brjansk area in southern Russia ingested, without her knowledge, 35.5 kBq of 137Cs in a single mushroom meal. Seven months later the woman became pregnant. Her total body content of 137Cs and 40K was measured regularly in a whole-body counter for three years following this intake. Data were thus available for the whole-body content for the periods before, during, and after pregnancy. Urine samples were collected regularly, and on two occasions breast milk was sampled. The 137Cs concentration in urine and breast milk was analyzed with a gamma-ray spectrometer. The body content of 137Cs decreased with a biological half-time of 107 d [95% confidence interval (CI): 106,109] before pregnancy, 58 d (95% CI: 53,64) during pregnancy, and 96 d (95% CI: 43,346) after the child was born. The ratio between the concentration of 137Cs in the urine (Bq/L urine) and in the body (Bq/kg body weight) increased during pregnancy from 18 +/- 6% to 35 +/- 6% (+/- 1 SD). The results show that there was a rapid decrease in the biological half-time of 137Cs at the beginning of the pregnancy and an increase after the child was born. The biological half-time during pregnancy was 54% of the half-time before pregnancy, which was reflected in the increased excretion of 137Cs in the urine. The ratio of the 137Cs concentration in breast milk to the whole body was 15% in the first month of breast-feeding. The effective dose, E, to the mother as a result from this intake was estimated to be 0.5 mSv, and the absorbed dose to the fetus was 0.06 mGy. These results are consistent with those reported elsewhere.     

几种微量元素对糖代谢的影响

饮食和生活方式对Ⅱ型糖尿病的预防发挥着重要作用,我们已知大量营养素(特别是脂肪和碳水化合物)和Ⅱ型糖尿病联系紧密,但对于微量营养素的作用还不够清楚。几项研究已经证实补充铜,硒,锌,铁和铬对胰岛素抵抗或糖尿病患者可能起到作用,研究它们之间的相互作用将为糖尿病的预防和辅助治疗提供更广阔的前景,而且尽可能的从食物中获得人体健康所需的微量元素应该是补充微量元素的最佳途径。     

Ethanol metabolism activates cell cycle checkpoint kinase, Chk2

Chronic ethanol abuse results in hepatocyte injury and impairs hepatocyte replication. We have previously shown that ethanol metabolism results in cell cycle arrest at the G2/M transition, which is partially mediated by inhibitory phosphorylation of the cyclin-dependent kinase, Cdc2. To further delineate the mechanisms by which ethanol metabolism mediates this G2/M arrest, we investigated the involvement of upstream regulators of Cdc2 activity. Cdc2 is activated by the phosphatase Cdc25C. The activity of Cdc25C can, in turn, be regulated by the checkpoint kinase, Chk2, which is regulated by the kinase ataxia telangiectasia mutated (ATM). To investigate the involvement of the regulators of Cdc2 activity, VA-13 cells, which are Hep G2 cells modified to efficiently express alcohol dehydrogenase, were cultured in the presence or absence of 25 mM ethanol. Immunoblots were performed to determine the effects of ethanol metabolism on the activation of Cdc25C, Chk2, and ATM. Ethanol metabolism increased the active forms of ATM and Chk2, as well as the phosphorylated form of Cdc25C. Additionally, inhibition of ATM resulted in approximately 50% of the cells being rescued from the G2/M cell cycle arrest and ameliorated the inhibitory phosphorylation of Cdc2. Our findings demonstrated that ethanol metabolism activates ATM. ATM can activate the checkpoint kinase Chk2, resulting in phosphorylation of Cdc25C and ultimately in the accumulation of inactive Cdc2. This may, in part, explain the ethanol metabolism–mediated impairment in hepatocyte replication, which may be important in the initiation and progression of alcoholic liver injury.