Food, intake

The acceptabihty of food is deterrnined by its flavor, and a large variety of industrial flavorings are used for the commercial preparation of foods. Most of the daily food intake, even in industrialized countries, contains flavor naturally or flavor formed during cooking and preparation for human consumption. Only a minor part of the daily food intake is covered by foods containing added flavorings. 

Meg estrolAceta.te. This compound is used outside the United States as an oral contraceptive. In the United States, it is used for the paUiative treatment of breast cancer and endometrial cancer, or as an adjunct to other therapies. Its use has been associated with an increased appetite and food intake and has been evaluated in the treatment of anorexia and cachexia (107). 

Oxygen, when introduced into fish-farming ponds and pools, particularly trout pools, enables these fish to increase their food intake and hence grow more rapidly (see Aquaculture chemicals). Fermentation operations are accelerated by sparging with oxygen (see Aeration,biotechnology Ferl ntation). 

Body mass variation for solids The variation in body mass due to food intake and subsequent excretion, in kg. 

Nahrungs-rohr, n., -rShre, /. alimentary canal, -sait, m. nutrient juice specif., (Med.) chyle, (Bot.) sap. -stoff, m. nutritive substance, nourishment, food. -stSrung, /. nutritional disturbance, -teilchen, n. nutritive element, -vergiftung, /. food poisoning, -wert, m. nutritive value, -zufuhr, /. food intake. 

It was shown to decrease the production of leptin and NPY and reduced food intake when administered to humans and rodents. 

Mood and hedonic value associated with feeding, food intake, foraging, consummatory behaviors, and craving in addiction complex regulation by food entrainable oscillators in the brain and periphery, neuropeptides (including orexins) and biogenic amines. 

Control of food intake Regulation of ingestive behaviour... 

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. 

Leptin is a cytokine produced and secreted by adipose tissue in proportion to the body fat content [3]. Mice and humans lacking leptin or its receptor develop a severe hyperphagia and a dramatic degree of obesity which is considerably more pronounced than that of the NDRKO mouse. Thus, leptin is the key adiposity signal in rodents and humans. Leptin secretion appears to reflect the metabolic status of the adipocyte rather than the sheer size of triglyceride deposits, and leptin levels may transiently be dissociated from total body fat. Nonetheless, over the course of a day with unrestricted food supply, plasma leptin levels reliably reflect the amount of total body fat. Local administration of leptin into the brain results in reduced food intake. The vast majority of patients with obesity have elevated serum levels of leptin. Thus, it is believed that the polygenic obesity is due to leptin resistance rather than to inadequate leptin secretion, or to a reduced blood/brain transport of the cytokine. 

Hormones, peptides and neurotransmitters Effect of ICV injection on food intake Effect of gene deletion on food intake Response to adiposity signals Receptor Effect of receptor defect on food intake... 

Schwartz MW, Woods SC, Porte D Jr et al (2000) Central nervous system control of food intake. Nature 404 661-671... 

CART (cocaine- and amphetamine-regulated transcript) is a hypothalamic peptide that inhibits both normal and starvation-induced feeding when injected into cerebral ventricles of rats. CART is co-localized with the anorexigenic peptide a-melanocyte-stimulating hormone in neurons of the arcuate nucleus. Secretion of CART is stimulated by leptin and CART may be an endogenous inhibitor of food intake. 

The cytokine leptin is secreted by adipocytes (fat cells) in proportion to the size of the adipose dq>ot and circulates via the bloodstream to the brain, where it ultimately affects feeding behavior, endocrine systems including reproductive function and, at least in rodents, energy expenditure. The major effect of Lqrtin is on the hy-pothalamous, where it suppresses appetite and hence food intake. Leptin exerts its effects via binding to the leptin receptor in the brain (specifically in the hypothalamus), which activates the JAK-STAT Pathway. 

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. 

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