During this last thirteen years, obesity’s incidence and its implication in metabolic and cardiovascular diseases and, more recently, cancer notably of fat submerged organs as stomac, pancreas, colon or kidneys, never stopped growing. But these epidemiological studies revealed an inconsistence if not a weakness of the correlation with the most widespread overweight indicator, the Body Mass Index.+
In the same time, fat revealed a functional and histologic heterogeneity between:
Thus, the first asserts itself as a masterchief of ernegetic homeostasis. It controls via the hypothalamus hunger and satiety, prevents and fights lipidic deposits in peripheral tissues (ectopy) and ensures with his metabolic flexibility energy expenditure, locomotor and brain activity, and body temperature regulation between meals. The second one, however, fades hunger and satiety through hypothalamus inflammation, promotes fat deposits generating steatosis, diabetes, cardiovascular diseases and nephropathy.
40 years ago appeared in research laboratories dwarf mice with an extraordinary longevity, 40 to 50% higher than that of wild mice. Those dwarf mice, named AMES and SNELL, which would have not survived outside the safety of laboratory cages, showed mutation on genes controlling the anterior pituitary gland territories which secretes growth hormones including GH, TSH and prolactin.+
The exploration of these mice revealed efficient physiological systems as a great insulin sensitivity and a reduced insulin signalling, a reduced GH/IGF-1 signalling, a decreased innate immunity, a great oxidative stress resistance associated to a high body detoxification capacity.
Yet, not only these physiological characteristics were found in all eukaryotes, from yeast to mammals including insects, but also in humans where, in the last ten years epidemiological studies on centenarians populations revealed the mutation frequency on the hGH/IFG-1 axis, the insulin signalling, and the oxidative stress and toxicants resistance capacity.
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