Within our sample showing low ghrelin levels probably related to the impaired nutritional status; patients with higher levels of ghrelin showed higher levels of alcohol craving. These preliminary data indicate that ghrelin could be implicated in the neurobiological mechanisms of alcohol craving, other than a hormone influenced by the nutritional status.

Aims/hypothesis Red blood cell distribution width (RDW) has been reported to be a risk marker of morbidity and mortality for cardiovascular disease in various study populations. However, no studies have investigated the relationship between RDW and diabetes complications. We therefore evaluated RDW as a marker of macrovascular and microvascular complications in a nationally representative sample of the adult diabetes population in the USA. Methods A cross-sectional study was performed using the nationwide 1988 to 1994 data set from the Third National Health and Nutrition Examination Survey. The association between RDW quartiles and macrovascular and microvascular complications was evaluated in 2,497 non-pregnant adults aged 20 years and older and affected by diabetes. Logistic regression modelling was used to adjust for potential confounding.

Animal studies suggest that the gut-brain peptide ghrelin plays an important role in the neurobiology of alcohol dependence (AD). Human studies show an effect of alcohol on ghrelin levels and a correlation between ghrelin levels and alcohol craving in alcoholics. This investigation consisted of two studies. Study 1 was a 12-week study with alcohol-dependent subjects, where plasma ghrelin determinations were assessed four times (T0-T3) and related to alcohol intake and craving [Penn Alcohol Craving Score (PACS) and Obsessive Compulsive Drinking Scale (OCDS)]. Serum growth hormone (GH) levels and assessment of the nutritional/metabolic status were also performed. Study 2 was a pilot case-control study to assess ghrelin gene polymorphisms (Arg51Gln and Leu72Met) in alcohol-dependent individuals. Study 1 showed no significant differences in ghrelin levels in the whole sample, while there was a statistical difference for ghrelin between non-abstinent and abstinent subjects. Baseline ghrelin levels were significantly and positively correlated with the PACS score at T1 and with all craving scores both at T2 and T3 (PACS, OCDS, obsessive and compulsive OCDS subscores). In Study 2, although there was a higher frequency of the Leu72Met ghrelin gene polymorphism in alcohol-dependent individuals, the distribution between healthy controls and alcohol dependent individuals was not statistically significant. This investigation suggests that ghrelin is potentially able to affect alcohol-seeking behaviors, such as alcohol drinking and craving, representing a new potential neuropharmacological target for AD.

BACKGROUND:Multiple genes that are associated with the risk of developing diabetes or the risk of diabetes complications have been identified by candidate gene analysis and genomewide scanning. These molecular markers, together with clinical data and findings from proteomics, metabolomics, pharmacogenetics, and other methods, lead to a consideration of the extent to which personalized approaches can be applied to the treatment of diabetes mellitus.CONTENT: Known genes that cause monogenic subtypes of diabetes are reviewed, and several examples are discussed in which the genotype of an individual with diabetes can direct considerations of preferred choices for glycemic therapy. The extent of characterization of polygenic determinants of type 1 and type 2 diabetes is summarized, and the potential for using this information in personalized management of glycemia and complications in diabetes is discussed. The application and current limitations of proteomic and metabolomic methods in elucidating diabetes heterogeneity is reviewed.

This study suggests that insulin could be involved in the neurobiology of alcohol craving and addiction. This characteristic seems specific of insulin since similar data were found on C-peptide but not on IGF-1. Future confirming studies on larger samples are needed, also to investigate possible therapeutic implications.

Restoration of lipid profile in CD patients after GFD treatment may be explained by an increase in both Apo-AI secretion by intestinal cells and body fat stores.

A relationship between alcohol craving and free T3 and TSH was demonstrated in AD patients, suggesting the potential involvement of the hypothalamic-pituitary-thyroid axis in the neurobiology of alcohol craving.

The benefits of low glycemic load (GL) diets on clinical outcome in several metabolic and cardiovascular diseases have extensively been demonstrated. The GL of a meal can be affected by modulating the bioavailability of carbohydrates or by changing food preparation. We investigated the effect on plasma glucose and insulin response in lean and obese women of adding raw or fried extra-virgin olive oil to a carbohydrate-containing meal. After an overnight fast, 12 obese insulin-resistant women (body mass index [BMI], 32.8 ± 2.2 kg/m(2)) and five lean subjects (BMI, 22.2 ± 1.2 kg/m(2)) were randomly assigned to receive two different meals (designated A and B). Meal A was composed of 60 g of pasta made from wheat flour and 150 g of grilled courgettes with 25 g of uncooked oil. Meal B included 15 g of oil in the 150 g of deep-fried courgettes and 10 g of oil in the 60 g of stir-fried pasta. Both meals included 150 g of apple. Blood samples were collected at baseline and every 30 minutes over a 3-hour post-meal period and were tested for levels of glucose, insulin, C-peptide, and triglycerides. The area under the curve (AUC) values were calculated. In obese women the AUCs for C-peptide were significantly higher after meal A than after meal B at 120 minutes (W [Wilcoxon sign rank test] = 27.5, P = .0020), 150 minutes (W = 26.5, P = .0039), and 180 minutes (W = 26.5, P = .0039). No differences were found in lean subjects. This study demonstrated that in obese, insulin-resistant women, food fried in extra-virgin olive oil significantly reduced both insulin and C-peptide responses after a meal.