Objective To compare appetite markers in reduced-obese individuals with a nonobese control group. Methods A total of 34 adults with obesity who lost 17% body weight at week 13 and maintained this weight loss (WL) at 1 year were compared with 33 nonobese controls matched for body composition. Basal and postprandial subjective appetite ratings and appetite-related hormone concentrations (ghrelin, total peptide YY, peptide YY3-36, total and active glucagon-like peptide 1, and cholecystokinin) were measured in all participants and repeated at week 13 and 1 year in the weight-reduced group. Results WL led to a reduction in prospective food consumption and an increase in feelings of hunger, fullness, and ghrelin secretion (basal and postprandial), but these new ratings were no different from those seen in controls. Postprandial concentrations of active glucagon-like peptide 1, total peptide YY, and cholecystokinin were lower in individuals with obesity at all time points compared with controls. Conclusion The increased drive to eat (both subjective feelings of hunger and ghrelin concentrations) seen in reduced-obese individuals, both after acute and sustained WL, reflects a normalization toward a lower body weight. Overall, WL does not have a sustained negative impact on satiety peptide secretion, despite a blunted secretion in individuals with obesity compared with nonobese controls.

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Food intake is a complex behavior regulated by discrete brain nuclei that integrate homeostatic nutritional requirements with the hedonic properties of food. Homeostatic feeding (i.e. titration of caloric intake), is typically associated with hypothalamic brain nuclei, including the paraventricular nucleus of the hypothalamus (PVN). Hedonic feeding is driven, in part, by the reinforcing properties of highly palatable food (HPF), which is mediated by the nucleus accumbens (NAc). Dysregulation of homeostatic and hedonic brain nuclei can lead to pathological feeding behaviors, namely overconsumption of highly palatable food (HPF), that may drive obesity. Both homeostatic and hedonic mechanisms of food intake have been attributed to several brain regions, but the integration of homeostatic and hedonic signaling to drive food intake is less clear, therefore we aimed to identify the neuroanatomical, functional, and behavioral features of a novel PVN → NAc circuit. Using viral tracing techniques, we determined that PVN → NAc has origins in the parvocellular PVN, and that PVN → NAc neurons express VGLUT1, a marker of glutamatergic signaling. Next, we pharmacogenetically stimulated PVN → NAc neurons and quantified both gamma-aminobutyric acid (GABA) and glutamate release and phospho-cFos expression in the NAc and observed a robust and significant increase in extracellular glutamate and phospho-cFos expression. Finally, we pharmacogenetically stimulated PVN → NAc which decreased intake of highly palatable food, demonstrating that this glutamatergic circuitry regulates aspects of feeding.

Foods high in phytochemicals are known for their role in the prevention of chronic disease development, but after processing and storage, such food products may lose part of their functionality as these compounds are sensitive to the impact of processing temperature and the type of methods applied. Therefore, we measured the levels of vitamin C, anthocyanins, carotenoids, catechins, chlorogenic acid, and sulforaphane in a complex blend of fruits and vegetables, and when applied to a dry food product, after exposure to different processing methods. These levels were compared between pasteurized, pascalized (high-pressure processing), and untreated conditions. Furthermore, we established the effect of freezing and storage time on the stability of these compounds. The results showed that pascalization better preserved vitamin C and sulforaphane, whereas pasteurization resulted in higher concentrations of chlorogenic acid, carotenoids, and catechins. For samples which were frozen and thawed immediately after processing, pascalization was the optimal treatment for higher contents of lutein, cyanidin-3-glucoside, quercetin-3-glucoside, delphinidin-3-glucoside, peonidin-3-glucoside, and epicatechin gallate. Ultimately, the optimal processing method to preserve phytochemicals in fruit and vegetable products is as complex as the blend of compounds, and this decision-making would best be led by the prioritized nutrient aim of an antioxidant food product.