TOXIC EFFECTS OF LARGE DOSE OF QUASSIN IN NORMAL AND DEPRIVED MICROFLORA RAT GROUPS

Eighteen rats were divided into three equal groups. The first group was closed orally with quassin, the second group was dosed with quassin after the gut flora were suppressed by difierent antibiotics, and the third group was served as a control. Food intake, water intake, and change in body weight were measured daily before dosing, during two weeks of dosing, and during one week after stopping dosing. Two eats from each group were killed at the end of each week, and stomach, liver, and kidney were collected for histopathologic examination. The results show a significant decline in daily food intake and daily change in body weight, and a significant increase in daily water intake in both dosed groups during the dosing period. Microscopic lesions were seen in the kidneys of both dosed rats group killed at the end of first and second week

Leptin and Beyond: Actors in Cancer

Leptin is a 16-kDa multifunctional, neuroendocrine peptide hormone secreted by adipocytes in proportion to total adipose tissue mass, known to control food intake, energy homeostasis, immune response, and reproductive processes [...]

What is the Impact of Energy Expenditure on Energy Intake?

Coupling energy intake (EI) to increases in energy expenditure (EE) may be adaptively, compensatorily, or maladaptively leading to weight gain. This narrative review examines if functioning of the homeostatic responses depends on the type of physiological perturbations in EE (e.g., due to exercise, sleep, temperature, or growth), or if it is influenced by protein intake, or the extent, duration, timing, and frequency of EE. As different measures to increase EE could convey discrepant neuronal or humoral signals that help to control food intake, the coupling of EI to EE could be tight or loose, which implies that some ways to increase EE may have advantages for body weight regulation. Exercise, physical activity, heat exposure, and a high protein intake favor weight loss, whereas an increase in EE due to cold exposure or sleep loss likely contributes to an overcompensation of EI, especially in vulnerable thrifty phenotypes, as well as under obesogenic environmental conditions, such as energy dense high fat—high carbohydrate diets. Irrespective of the type of EE, transient elevations in the metabolic rate seem to be general risk factors for weight gain, because a subsequent decrease in energy requirement is not compensated by an adequate adaptation of appetite and EI.

Brain adiponectin signaling controls peripheral insulin response in Drosophila

The brain plays a key role in energy homeostasis, detecting nutrients, metabolites and circulating hormones from peripheral organs and integrating this information to control food intake and energy expenditure. Here, we show that a group of neurons in the Drosophila larval brain expresses the adiponectin receptor (AdipoR) and controls systemic growth and metabolism through insulin signaling. We identify glucose-regulated protein 78 (Grp78) as a circulating antagonist of AdipoR function produced by fat cells in response to dietary sugar. We further show that central AdipoR signaling inhibits peripheral Juvenile Hormone (JH) response, promoting insulin signaling. In conclusion, we identify a neuroendocrine axis whereby AdipoR-positive neurons control systemic insulin response.

Mathematical Modelling of Diet Planning Problem for Hypertension Patients

Hypertension or high blood pressure is also called a “silent killer” that may lead to serious damage to the heart and kidney. The worst case can result in sudden death. Unbalanced diets are one of the risk factors for hypertension. Previous studies have proven that diet plays a significant role in influencing hypertension patient condition. Proper planning on the selection of diets needs to be done to control food intake for this cardiovascular disease patient. This study aims to formulate a mathematical model of diet planning for hypertension patients. Specifically, this study attempts to determine the amount of nutrients need by hypertension patients, to find the cost of the food combination, and to identify the best model between linear programming and integer programming. The research model included 10 types of food groups with 200 variables based on Malaysian recipes and developed a mathematical model using two programming techniques; linear programming and integer programming. The finding showed that the solution provided by the entire programming method has met the constraints and requirements of the food group. The results from the integer programming approach would offer optimal and efficient alternatives to diet planning for patients with hypertension. It can serve as a guideline for hypertension patients on type of food to eat and the correct amount of serving to complete their nutritional plan.

Hypothalamic Expression of Neuropeptide Y (NPY) and Pro-OpioMelanoCortin (POMC) in Adult Male Mice Is Affected by Chronic Exposure to Endocrine Disruptors

In the arcuate nucleus, neuropeptide Y (NPY) neurons, increase food intake and decrease energy expenditure, and control the activity of pro-opiomelanocortin (POMC) neurons, that decrease food intake and increase energy expenditure. Both systems project to other hypothalamic nuclei such as the paraventricular and dorsomedial hypothalamic nuclei. Endocrine disrupting chemicals (EDCs) are environmental contaminants that alter the endocrine system causing adverse health effects in an intact organism or its progeny. We investigated the effects of long-term exposure to some EDCs on the hypothalamic NPY and POMC systems of adult male mice that had been previously demonstrated to be a target of some of these EDCs after short-term exposure. Animals were chronically fed for four months with a phytoestrogen-free diet containing two different concentrations of bisphenol A, diethylstilbestrol, tributyltin, or E2. At the end, brains were processed for NPY and POMC immunohistochemistry and quantitatively analyzed. In the arcuate and dorsomedial nuclei, both NPY and POMC immunoreactivity showed a statistically significant decrease. In the paraventricular nucleus, only the NPY system was affected, while the POMC system was not affected. Finally, in the VMH the NPY system was affected whereas no POMC immunoreactive material was observed. These results indicate that adult exposure to different EDCs may alter the hypothalamic circuits that control food intake and energy metabolism.

The Function of Gastrointestinal Hormones in Obesity—Implications for the Regulation of Energy Intake

The global burden of obesity and the challenges of prevention prompted researchers to investigate the mechanisms that control food intake. Food ingestion triggers several physiological responses in the digestive system, including the release of gastrointestinal hormones from enteroendocrine cells that are involved in appetite signalling. Disturbed regulation of gut hormone release may affect energy homeostasis and contribute to obesity. In this review, we summarize the changes that occur in the gut hormone balance during the pre- and postprandial state in obesity and the alterations in the diurnal dynamics of their plasma levels. We further discuss how obesity may affect nutrient sensors on enteroendocrine cells that sense the luminal content and provoke alterations in their secretory profile. Gastric bypass surgery elicits one of the most favorable metabolic outcomes in obese patients. We summarize the effect of different strategies to induce weight loss on gut enteroendocrine function. Although the mechanisms underlying obesity are not fully understood, restoring the gut hormone balance in obesity by targeting nutrient sensors or by combination therapy with gut peptide mimetics represents a novel strategy to ameliorate obesity.

Role of Nutrient and Energy Sensors in the Development of Type 2 Diabetes

Cell survival depends on the constant challenge to match energy demands with nutrient availability. This process is mediated through a highly conserved network of metabolic fuel sensors that orchestrate both a cellular and whole-body energy balance. A mismatch between cellular energy demand and nutrient availability is a key factor in the development of type 2 diabetes, obesity, metabolic syndrome, and other associated pathologies; thus, understanding the fundamental mechanisms by which cells detect nutrient availability and energy demand may lead to the development of new treatments. This chapter reviews the role of the sensor PASK (protein kinase with PAS domain), analyzing its role in the mechanisms of adaptation to nutrient availability and the metabolic response in different organs (liver, hypothalamus) actively cooperating to control food intake, maintain glycaemia homeostasis, and prevent insulin resistance and weight gain.