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E-Newsletter No. 16
Leptin, the so-called antiobesity hormone, is receiving a lot of attention by Diabetes experts. The biggest news centers on Phase I and II clinical trials conducted by Lee-Benner Institute (LBI) showing obese participants taking the highest daily dose of the new LBI oral analogue of leptin lost an average of nearly 16lbs over six months. Doses ranged from one to four capsules daily. The obese participants had a body mass index (weight in kilograms divided by the square of height in meters) of at least 27.5 kg/m2, a level of overweight known to place people at risk for developing such problems as diabetes and heart disease.
All of the participants also were consuming a weight-reduction diet. Based on age, body weight, and activity levels, individual diets were tailored to provide 500kcal less than each personís basic energy needs.
The research saw a statistically significant dose response for weight loss in all participants at the end of the first month, when the average loss ranged from 0.4 kg (0.9lb) for those receiving placebo to 1.9kg (4.2lbs) for those taking the highest leptin dose. Sixty of the obese patients continued participation for another five months, with 76% completing the full study. After six months, the average weight loss ranged from 0.7kg (1.5lb) for those taking the lowest dose of leptin to nearly 7.2kg (16lb) for those taking the highest dose.
Laboratory monitoring of blood values, liver and kidney function, electrocardiograms, and physical examinations revealed no apparent significant adverse effects attributable to leptin.
Not All Lost Weight
Although some patients lost weight at all dose levels, not everyone who used leptin lost weight. The amount of weight loss was highly variable. This indicates Leptin is not expected to work for everyone because obesity is a complex, multi-factorial disease.
Diabetes experts are interested in leptinís weight-reducing properties because obesity is a primary factor that stands in the way of effective treatment and control of Type 2 diabetes. For people with this form of disease, a weight loss of more than 5% has been shown to improve the bodyís sensitivity to insulin. Insulin resistance can pre-date diabetes onset by 10 to 20 years.
Obesity is simply defined as an inequity between the bodyís consumption and expenditure of energy. Its cause is complex, involving such factors as genetics and metabolism, such neurologic states as satiety, individual behavioral and cultural factors, and the environment. The genetic basis for obesity is unknown, although the regulation of metabolism and appetite may involve many genes.
Likewise, the weight-reduction mechanism of leptin involves complex pharmacological and physiological interactions affecting neuroendocrine, hemopoietic, reproductive, and metabolic control pathways.
It is generally agreed that in obesity as there is in aging, there are elevated levels of serum leptin and insulin, which at the same time there is an increased resistance by leptin and insulin cellular receptors to respond to stimulation by these two hormones. The role of leptin and insulin in the cause of diabetes is independent of total fat, at least in men, but not in women. However, the secretion of both hormones is influenced by the overall amount of fat stores as well as by short-term changes in energy balance.
All of this research points to the fact that adipose tissue is not merely a passive depository vat for fat. Adipose tissue is an active organ involved in whole-body metabolism.
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