Green tea extract improves high fat diet-induced hypothalamic inflammation, without affecting the serotoninergic system.

To investigate possible mechanisms of green tea's anti-obesity and anti-diabetic effects in the hypothalamus, the central regulator of metabolism, of mice fed with high-fat diet (HFD), we analyzed proteins of the toll-like receptor 4 (TLR4) pathway and serotoninergic proteins involved in energy homeostasis. Thirty-day-old male Swiss mice were fed with HFD rich in saturated fat and green tea extract (GTE) for 8 weeks. After that, body weight and mass of fat depots were evaluated. Oral glucose tolerance test was performed 3 days prior to euthanasia; serum glucose, insulin and adiponectin were measured in fasted mice. Hypothalamic TLR4 pathway proteins, serotonin receptors 1B and 2C and serotonin transporter were analyzed by Western blotting or enzyme-linked immunosorbent assay. A second set of animals was used to measure food intake in response to fluoxetine, a selective serotonin reuptake inhibitor. Mice fed with HFD had increased body weight and mass of fat depots, impaired oral glucose tolerance, elevated glucose and insulin and decreased adiponectin serum levels. TLR4, IκB-α, nuclear factor κB p50 and interleukin 6 were increased by HFD. Concomitant GTE treatment ameliorated these parameters. The serotoninergic system remained functional after HFD treatment despite a few alterations in protein content of serotonin receptors 1B and 2C and serotonin transporter. In summary, the GTE attenuated the deleterious effects of the HFD investigated in this study, partially due to reduced hypothalamic inflammation.

[Foods and nutrients modulates the release of anorexigenic gastrointestinal hormones]. / Alimentos e nutrientes modulam a libertação de hormonas intestinais anorexígenos.

The short-term regulation of food intake controls what, how much and when we eat during one day or a single meal. When ingested, the nutrients produce satiety by means of mechanic stimulation and hormonal release. Many of these hormones also inhibit gastric empting and increase the gastric mechanoreceptor stimulation. The present review of the literature focuses on the effect of different food and nutrients on the release of anorexigenic regulators of food intake, as polypeptide insulinotropic glucose dependent, oxyntomodulin, peptide YY, cholecystokinin, and glucagon-like peptide 1.

Long-term nutrition education reduces several risk factors for type 2 diabetes mellitus in Brazilians with impaired glucose tolerance.

The aim of this study was to evaluate the effects of a nutrition education program (NEP) on anthropometric, dietetic, and metabolic parameters in high-risk subjects for type 2 diabetes mellitus. Fifty-one participants, both sexes, were randomly assigned to either the control (58.8%) or the intervention (NEP) group. The intervention group received frequent individual and group nutritional counseling from a team of nutritionists. Participants were assessed at baseline (M0) and after 12 months (M1) for anthropometric, dietetic, and metabolic parameters. The hypothesis was that high-risk subjects for type 2 diabetes mellitus participating in NEP would show an improvement in these parameters. At M1, the intervention group showed a significant decline in body weight (-3.4%), body mass index (-5.7%), cholesterol intake (-49.5%), fasting glycemia (-14.0%), fasting insulin (-9.0%), postprandial glycemia (-21.0%), postprandial insulin (-71.0%), total serum cholesterol (-23.0%), and glycated hemoglobin (-24.0%). A decrease in energy intake (5%, P = .06) and low-density lipoprotein cholesterol (25%, P = .07) was observed in the interventional group, although it did not reach statistical significance. In contrast, the control group presented a significantly higher energy intake (19%, P = .04) and a nonsignificant increase in consumption of all macronutrients. The long-term NEP was found to improve anthropometric, dietary, and metabolic parameters in high-risk subjects for type 2 diabetes mellitus.

Prolonged consumption of soy or fish-oil-enriched diets differentially affects the pattern of hypothalamic neuronal activation induced by refeeding in rats.

We used c-Fos immunoreactivity to estimate neuronal activation in hypothalamic feeding-regulatory areas of 3-month-old rats fed control or oil-enriched diets (soy or fish) since weaning. While no diet effect was observed in c-Fos immunoreactivity of 24-h fasted animals, the acute response to refeeding was modified by both hyperlipidic diets but with different patterns. Upon refeeding, control-diet rats had significantly increased c-Fos immunoreactivity only in the paraventricular hypothalamic nucleus (PVH, 142%). In soy-diet rats, refeeding with the soy diet increased c-Fos immunoreactivity in dorsomedial hypothalamic nucleus (DMH, 271%) and lateral hypothalamic area (LH, 303%). Refeeding fish-diet rats with the fish diet increased c-Fos immunoreactivity in PVH (161%), DMH (177%), VMH (81%), and ARC (127%). Compared to the fish-diet, c-Fos immunoreactivity was increased in LH by the soy-diet while it was decreased in ventromedial hypothalamic nucleus (VMH) and arcuate hypothalamic nucleus (ARC). Based on the known roles of the activated nuclei, it is suggested that, unlike the fish-diet, the soy-diet induced a potentially obesogenic profile, with high LH and low VMH/PVH activation after refeeding.