Influence of BMI and gender on postprandial hormone responses. Obesity. 2007;15:2974 -2983. Objective: Influences of gender and body weight on the hormonal response to eating are not well understood. This study was conducted to determine a convenient time-point to evaluate peak postprandial hormone responses and to test the hypothesis that gender and BMI interact to produce differences in postprandial secretion of selected humoral markers implicated in hunger and satiety. Research Methods and Procedures: Fasting blood glucose, insulin, leptin, ghrelin, glucagon-like peptide-1, and glucagon were measured in normal-weight (20 Յ BMI Ͻ 25 kg/m 2 ) men (n ϭ 10) and women (n ϭ 9) and obese (BMI Ն 30 kg/m 2 ) men (n ϭ 9) and women (n ϭ 11). A standard liquid meal was consumed, and humoral measurements were repeated every 10 minutes for 1 hour. Data were analyzed using repeated measures ANOVA with BMI and gender as main effects. Results: Obese subjects had delayed peak insulin responses (p ϭ 0.004), whereas obese men had a delayed nadir ghrelin response (p ϭ 0.05). Obese subjects had higher and more sustained postprandial glucose (p ϭ 0.02), and greater fasting (p ϭ 0.0004) and postprandial insulin (p ϭ 0.0001). Ghrelin decreased after the meal (p ϭ 0.003); the percent change from fasting tended to be reduced in obese subjects (p ϭ 0.07). Men had greater fasting (p ϭ 0.02) and postprandial (p ϭ 0.03) glucagon and a subtle postprandial decline in plasma leptin (p ϭ 0.01). Discussion: Peak hormone responses occurred 20 to 40 minutes after eating. Measurements made during this interval may be useful in evaluating postprandial response magnitude. Peak/nadir responses and time courses of postprandial responses are influenced by gender and BMI. Nutritional studies need to account for variability introduced by these factors.

Processes such as aberrant redox signaling and chronic low-grade systemic inflammation have been reported to modulate age-associated pathologies such as cognitive impairment. Curcumin, the primary therapeutic component of the Indian spice, Turmeric (Curcuma longa), has long been known for its strong anti-inflammatory and antioxidant activity attributable to its unique molecular structure. Recently, an interest in this polyphenol as a cognitive therapeutic for the elderly has emerged. The purpose of this paper is to critically review preclinical and clinical studies that have evaluated the efficacy of curcumin in ameliorating and preventing age-associated cognitive decline and address the translational progress of preclinical to clinical efficacy. PubMed, semantic scholar, and Google scholar searches were used for preclinical studies; and clinicaltrials.gov , the Australian and New Zealand clinical trials registry, and PubMed search were used to select relevant completed clinical studies. Results from preclinical studies consistently demonstrate curcumin and its analogues to be efficacious for various aspects of cognitive impairment and processes that contribute to age-associated cognitive impairment. Results of published clinical studies, while mixed, continue to show promise for curcumin's use as a therapeutic for cognitive decline but overall remain inconclusive at this time. Both in vitro and in vivo studies have found that curcumin can significantly decrease oxidative stress, systemic inflammation, and obstruct pathways that activate transcription factors that augment these processes. Future clinical studies would benefit from including evaluation of peripheral and cerebrospinal fluid biomarkers of dementia and behavioral markers of cognitive decline, as well as targeting the appropriate population.

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These data indicate that 6 months after LGBS there were significant improvements in many cardiovascular and metabolic risk markers. However, VAT reduction was most strongly associated with reductions in insulin resistance. Body weight loss was not associated with markers of improved insulin sensitivity.