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Sibutramine was originally developed as an anti depressant and it inhibits the reuptake of noradrenaline and serotonin at nerve endings, increasing the concentration of these neurotransmitters at postsynaptic receptors in the brain that affect food intake. It is also thought to stimulate energy expenditure.

The drug is rapidly absorbed from the gastrointestinal tract and extensively metabolised in the liver by cytochrome P450 3A4. These metabolites have a t1/, of 14-16 h and are responsible for its effects.

When taken with dietary advice, sibutramine can be expected to cause a loss of 5-7% of initial body weight but this tends to be regained once the drug is stopped.

Sibutramine should be prescribed only for individuals with BMI 27 kg/m2 or more who have other cardiovascular risk factors or 30 kg/m2 or more in their absence. It should be discontinued if weight loss after 3 months is < 5% of initial weight, if weight stabilises at < 5% of initial weight thereafter or if users regain more than 3 kg after previous weight loss. It should not be given for more than 1 year.

The dose is 10-15 mg day by mouth.

Adverse effects include constipation, dry mouth and insomnia which occur in > 10% of users. Less commonly, nausea, tachycardia, palpitations, raised blood pressure, anxiety, sweating and altered taste may occur. Blood pressure should be monitored closely throughout its use (twice weekly in the first 3 months). Contraindications include severe hypertension, peripheral occlusive arterial or coronary heart disease, cardiac arrhythmia, prostatic hypertrophy and those with severe hepatic or renal impairment. It should not be used to treat obesity of endocrine origin or those with a history of major eating disorder or psychiatric disease. Concomitant use with tricyclic antidepressants should be avoided (CNS toxicity).

The noradrenergic drugs fenfluramine, dexfen-fluramine and phenteramine were formerly prescribed as appetite suppressants but were withdrawn when their use was associated with cardiac valve disease and pulmonary hypertension.

Considerable interest continues to surround the adipocyte-derived hormone leptin (Greek, leptos, thin) which acts on the hypothalamus to control appetite and energy expenditure by informing neuroendocrine pathways of the state of energy stores in adipose tissue. Plasma leptin correlates with indices of obesity in humans, with most obese patients being resistant to their elevated levels of leptin, rather than deficient in leptin production. The use of therapeutic doses of leptin is under evaluation; physiological doses are effective in rare patients with inherited leptin deficiency. Further understanding of the leptin pathway may open avenues for new agents to control appetite and obesity.

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