THE FAT LOSS: HYPOTHALAMIC REGULATION
The function of the hypothalamus is critical for body weight regulation. Research with rats has shown that damage to the hypothalamus can have serious consequences. Damage to the ventromedial hypothalamus (VMH) is associated with hyperphagia (over-eating), decreased thermogenesis and spontaneous aotrvity, and elevated insulin levels. Obesity is almost an inevitable result! On the other hand, destruction of the lateral hypothalamus, only microns away, is associated with decreased food intake and a reduction in body fat.
These changes are partly influenced by the actions of chemical messengers, called neurotransmitters. Different types of neurotransmitters function to stimulate specific areas of the brain responsible for certain mental states. There are a number of neurotransmitters that can either promote or discourage feeding. For example, seratonin, derived from the amino acid tryptophan, can reduce food intake and this is now the basis of several appetite-suppressing drugs. Ingestion of carbohydrate results in the release of seratonin which inhibits the norther intake of food. Conversely, another neurotransmitter in the brain, neuropeptide Y, stimulates food consumption. There are a number of other chemical messengers that either stimulate or inhibit food intake—the strength of specific signals after a preferred food has been eaten may affect that food’s desirability for further consumption.
Isolation of a ’satiety’ gene, by geneticists working at Rockefeller University in 1994, suggests that genetics may play an important part in hunger. Research carried out over several years has suggested there may be a mechanism coded for by a gene or genes, which ’switches off hunger signals in the hypothalamus. Scientists have searched for, found, and now synthesised a protein hormone which they have called ‘teptin’ Qeptos is Greek for ‘thin’ which may result in major advances for drug therapy for obesity—if it lives up to its early promises.
In addition to dealing with neurotransmitter signals and proteins, the hypothalamus integrates a wide variety of messages, from the first smell of food to its metabolic fate as stored energy, by a series of neurotransmitters, hormones and signals from circulating nutrients.
Physiological signals—Stomach and intestinal distension are mechanisms for terminating feeding by negative feedback via the nervous system. The release of hormones such as cholecystokimn and the stirnulation of special receptors in the gut also provide signals to reduce feeding.
Nutrient -Circulating glucose, amino adds and may also signify that food has entered the body’s system and reduce the desire to eat. Low blood sugar levels promote hunger and it is possible that lesser degrees of changes in blood sugar may also influence appetite mechanisms.
Hormonal signals—A variety of hormonal changes occur in response to ingested and absorbed nutrients and some of these may influence appetite mechanisms. Insulin is one of the main hormones involved in nutrient metabolism but its role in appetite mechanisms has not been clearly identified.
Metabolic signals—The conversion of nutrients into storage tissues may influence appetite mechanisms. For example, the amount of carbohydrate and glycogen stores or fat in adipose tissue may feed back signals to the hypothalamus, giving it important information about the status of the body’s energy reserves.
From this wealth of feedback the brain must sort out relevant signals and make decisions about food intake. When hunger is high, an individual’s ability to inhibit inappropriate food choices is reduced. Many food companies, especially snack food manufacturers, exploit this by advertising their products on television around meal-times.
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