Wednesday November 25 2009 | Biotechnology feed | All feeds
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Wednesday November 25 2009 | Biotechnology feed | All feeds
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Exploiting the anorectic and insulin sensitizing activity of endogenous leptin It is estimated that somewhere between 34 and 61 million people in the US are obese and in much of the developing world incidence is increasing by about 1% per year. Obesity increases the likelihood of death from all causes by 20%, and more specifically death from coronary artery disease and stroke are increased by 25% and 10% respectively. Key priorities of anti-obesity treatments are to reduce food intake and/or hyperlipidemia however molecules that have the additional effect of reducing insulin resistance, a primary factor contributing to the development of diabetes, would have added benefit. In a recent dossier overviewing therapeutic targets developed to break the link between obesity and diabetes (click here for access) we feature leptin agonists. This class of drugs not only has the potential to break this link but they are also potent anorectics in a number of animal models. Despite the potential of such drugs their efficacy has been brought into doubt by the observation that patients are obese even in the context of high levels of endogenous leptin suggesting that these individuals develop a resistance to leptin. Swiss researchers have recently investigated this phenomenon. Serum IL-1Ra concentrations were reported to be elevated 6.5-fold in obese subjects, and this correlated with insulin resistance. IL-1Ra has been shown to antagonize the action of leptin at the hypothalamic level in rodents, thereby inducing leptin resistance. It therefore appears likely that a similar phenomenon occurs in humans. Strategies that are able to reduce the levels of IL-1Ra may therefore allow the high levels of leptin found in obese patients to translate to anorectic activity and reduced insulin resistance. Link to journal abstract:
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