Leptin

Leptin         In the mid 1980s Amgen bought the rights to study the leptin molecule, the key regulator of fat stores. It was thought to have peachy potential for treating obesity. The innervation surrounding leptin was ground on several studies that showed that when leptin was injected into mice and rats with genetically based obesity, it caused them to decrease food intake and drop to a expression weight with no side effects. The naughtyer the leptin levels in the source serum, the more pronounced the effect was. There seemed to be great potential for therapeutic uses of leptin. A setback occurred with the finding that closely spate with non-genetically based obesity had higher than normal levels of leptin in their blood, which would seem to be in conflict with the weight-reducing effect of high leptin in the rodent studies. It was theorized that obese people might execute resistant to their sustain leptin in a way akin to obese people who develop diabetes because they become resistant to their own insulin. Subsequent clinical trials where leptin was administered to obese people showed no noteworthy weight loss. It was thought that leptin was not crossing the blood-brain barrier in lay to affect its target organ, the brain.

Leptin Regulation:         Leptin is a 16 kDa protein expressed exclusively in adipose tissue.



It is a endocrine that communicates the status of energy stores to the hypothalamus. Higher leptin levels correlate with energy intake and low leptin levels correlate with energy saving (2-4; 12-15). Low leptin levels ar found in rodents with the leptin gene (ob gene) knocked out and in people with mutations in the ob gene (14).

        Several factors contribute to leptin levels. The nearly important contribution is the amount of body fat, but age, gender, hormones and cytokine levels in addition have an effect...

If you want to get a full essay, order it on our website: Ordercustompaper.com



If you want to get a full essay, wisit our page: write my paper