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Background: Body energy homeostasis is largely regulated by the interactions between appetite-related brain regions and gut hormones. Objective: We hypothesized that the sensitivity of appetite-related brain regions [eg, hypothalamus, insula, thalamus, parahippocampal/ hippocampal cortex, caudate, putamen, amygdala, and orbitofrontal cortex (OFC)] varies for each macronutrient, and the differential sensitivity is associated with gut hormone concentrations in humans. Design: Brain activation responses to ingested fat, glucose, protein, and water in the above-mentioned 8 brain regions of 14 healthy men were investigated by using functional magnetic resonance imaging. Fasting and postprandial plasma glucose, insulin, ghrelin, cholecystokinin (CCK), and glucagon-like peptide 1 (GLP-1) concentrations were measured. The relation of the blood oxygen level-dependent (BOLD) signal with plasma glucose and hormone concentrations was assessed by using Pearson's correlation analysis. Results: Ingested macronutrients similarly reduced the BOLD signal in the middle insula, thalamus, parahippocampal cortex, caudate, and lateral OFC. Protein ingestion reduced the BOLD signal in the amygdala more effectively than did fat and glucose ingestion. BOLD signal changes were positively correlated with circulating ghrelin concentrations and were negatively correlated with circulating insulin, CCK, and GLP-1 concentrations. The findings indicate variations in the correlation between brain activation and plasma hormone concentrations after ingestion of different macronutrients. Conclusions: The middle insula, thalamus, parahippocampal cortex, caudate, and lateral OFC, but not the amygdala, have similar sensitivities, to isocaloric and isovolumetric macronutrient solutions. Differential correlations exist between BOLD signal changes in activated brain regions and postprandial changes in plasma concentrations' of different gut hormones in response to the ingestion of different macronutrients. [ABSTRACT FROM AUTHOR]

Background: Mastication is the first step in ingesting food, but the effects of mastication on energy intake and gut hormones in both obese and lean subjects have not been extensively evaluated. Objective: The current study aimed to compare the differences in chewing activities between obese and lean subjects and to examine the effects of chewing on energy intake and gut hormone concentrations in both obese and lean subjects. Design: Sixteen lean and 14 obese young men participated in the current research. In study 1, we investigated whether the chewing factors of obese subjects were different from those of lean subjects. In study 2, we explored the effects of chewing on energy intake. A test meal consisting of 2200 kJ (68% of energy as carbohydrate, 21% of energy as fat, and 11% of energy as protein) was then consumed on 2 different sessions (15 chews and 40 chews per bite of 10 g of food) by each subject to assess the effects of chewing on plasma gut hormone concentrations. Results: Compared with lean participants, obese participants had a higher ingestion rate and a lower number of chews per 1 g of food. However, obese participants had a bite size similar to that of lean subjects. Regardless of status, the subjects ingested 11.9% less after 40 chews than after 15 chews. Compared with 15 chews, 40 chews resulted in lower energy intake and postprandial ghrelin concentration and higher postprandial glucagon-like peptide 1 and cholecystokinin concentrations in both lean and obese subjects. Conclusion: Interventions aimed at improving chewing activity could become a useful tool for combating obesity. [ABSTRACT FROM AUTHOR]

Sulforaphane (SFN), mainly derived from cruciferous vegetables, has received much attention for its cancer chemopreventive property. Though there have been a few epidemiological studies supporting its beneficial effect on cardiovascular diseases, much experimental evidence are still required to understand its mechanism. In this study, human vascular endothelial cell, a barrier of blood, was used as an in vitro model to investigate the protective effect of sulforaphane on inflammatory damage induced by lipopolysaccharide (LPS). The results showed that sulforaphane inhibited the expression of COX-2 and iNOS stimulated by lipopolysaccharide in a dose- and time-dependent manner. Moreover, sulforaphane suppressed the phosphorylation of ERK1/2, JNK, and p38 activated by lipopolysaccharide. Pretreatment with SB202190, the specific inhibitor of p38, abolished the expression of COX-2 induced by LPS. Likewise, SP600125, inhibitor of JNK, abrogated iNOS expression stimulated by LPS. Moreover, pretreatment with anisomycin (AM), an activator of p38 and JNK, instead of LPS, the expression of COX-2 and iNOS is still inhibited by sulforaphane. Interestingly, SFN significantly induced HO-1 and TR expression down-regulated by LPS. Taken together, these data indicated that sulforaphane exhibited the protective role against the inflammatory injury in vascular endothelia cells, through inactivating p38 MAPK and JNK, as well as inducing phase 2 enzymes. [ABSTRACT FROM AUTHOR]