Persistent Insulin Resistance, A Hindrance to Optimal Health over Many Years

At this point, it seems somewhat necessary to describe the background behind IR in more detail, because history reveals in actuality the only real well-developed role of chromium is to enhance insulin sensitivity—using other words, to ameliorate IR. Despite limitations in applicability, this single recognized role is extremely important. IR has received much recently well-deserved respect for its role in optimal health by both professionals and the lay public. Many differing chronic metabolic disorders are becoming more widespread and severely damaging in the aging populations, and much of this can be attributed to the progression of the health perturbation referred to as IR [5,6,30-32].

A century ago after the isolation and purification of insulin by Banting and colleagues, it was largely insinuated that diabetes, an abnormal escalation in circulating glucose, was wholly due to a deficiency of circulating insulin [33]. So, the general conviction was that diabetes was quite curable because lack of insulin could now be handled. However, another form of diabetes was soon discovered when it was noted that an unexpected increase of insulin in the bloodstream was frequently present despite abnormally high circulating glucose concentrations [4]. Ironically, this picture eventually became more common than diabetes originally described with diminished insulin circulation—type 1. Thus, this more common form attributed greatly to the above-mentioned IR was naturally referred to as diabetes mellitus type 2. Worth repetition, IR is generally accepted to be a critical driving force behind the linked constituents of MS including NAFLD [5,6,34-36].

In “endocrine terms,” what precisely is IR? Similar to the thyroid and adrenals as endocrine systems, the glucose-insulin system has many compensatory capabilities. Specifically, it also has distinctive responses to any diminution in hormonal activity. In the case of IR, a general tendency exists under certain conditions for peripheral target tissues such as liver, fat, and muscle to experience a lessened, apparently sub-optimal response to insulin over time. To compensate for the lower activity, more insulin is produced and released from the pancreas as its compensatory response. While this benefit has some merit by returning circulating glucose more toward optimum, the final outcome is to impose higher circulating glucose and insulin levels than prior that can be potentially harmful presently and in the future [17,18]. Such occurrences have been given a unique nomenclature, explicitly “trade off’ because they can create instant benefits but future harms [37]. As the organ resistance to insulin continues to chronically become more severe, the prolongation of the interplay between glucose and insulin can continue to unfold. Hence, both levels of circulating glucose and insulin may elevate more and more and be associated with increasing prevalence and severity of the risk factors leading to the plethora of disorders associated with diabetes type 2, MS, and NAFLD [7,17]. In fact, there is some possibility that not maintaining an optimal glucose- insulin system could lead to a shorter, unhealthier lifespan [17,18]. So, it should be obvious that the desire of DeFronzo and Ferrannini to develop a safe, effective insulin sensitizer would be most beneficial [7].

 
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