Abstract
The galloping incidence and the alarming prevalence of Metabolic Syndrome (MbS) has put the human life on the edge of a certain catastrophe. Despite the full-blown epidemic presentation and ongoing and ever-expanding list of clinical and biochemical manifestations of the syndrome, not much have been logically addressed with regard to a comprehensive pathogenesis and an integrated etiology. What we have so far heard about MbS is more or less like the old Indian tale of examining a huge elephant in the dark. We would like to open a small but sun-view window and shed a faint beam of light onto this perplexing issue, and puzzle out the neglected pieces of a semiset picture and carry the current concepts regarding MbS one big step further. It is crystal clear that, metabolic syndrome is not merely a metabolic disorder, but also a real chaos at the level of molecular biology and inter-cellular dialogue; a state of generalized cell swelling, cell refreshing defect, cell senescence, chronic oxidative stress, and derailed tissue remodeling due to diverse unusual tissue growth factor expressions. Opposite to common belief of over- feeding and obesity as the initiating factor of metabolic syndrome, we suggest that a world-wide ubiquitous environmental insult has led to a state of profound signal-receptor mal-engagement and misunderstanding; an all-out syndrome which is unequivocally tied up to a strange and totally new pattern of insulin resistance state being emerged out of real blue in late 1980s. What we are trying to propose is that, the centripetal obesity of metabolic syndrome is the result of a recently broken out overwhelming insulin resistance state and its reciprocal, compensatory hyperinsulinemia, not simply and solely the cause of it. We would like to argue that in metabolic syndrome the insulin resistance comes first and leads to central adiposity. At the end, an all-embracing environmental risk factor will be logically hinted at as a novel etiologic clue.
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