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Bromocriptine-QR (Cycloset)

Investigating the connection between neuroendocrine regulation of the biological clock system and its subsequent regulation of physiology to determine if an environmentally imposed derangement of clock regulation such as modern western life style may influence metabolism and metabolic disease.

A New Paradigm in the Understanding and Treatment of the Metabolic Syndrome, Part 2

As concluded in the previous newsletter in this series, “Evolutionary selection for insulin resistance in a cyclic environment: brain clocks and control of peripheral metabolism” the brain is equipped with circadian neurophysiological mechanisms to induce (and reverse) the insulin resistant state that evolved as a survival strategy against ensuing environmental stresses such as prolonged (seasonal) lack of food availability. A central facilitator of this insulin resistance induction is a diminution of the circadian peak in dopaminergic activity at the SCN. Neurotoxin induced destruction of these dopaminergic projections to the clock of insulin sensitive animals induces marked insulin resistance and glucose intolerance without alterations in food consumption.

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A New Paradigm in the Understanding and Treatment of the Metabolic Syndrome: Targeting Alterations within the Biological Clock System

The prevalence of obesity and insulin resistance syndrome, rare only a century ago in most geographic locals of the world are now disorders whose prevalence represents the majority of humans in westernized countries on planet Earth. This simple observation strongly suggests that factors other than or in addition to genetic mutations/alterations are facilitating this rapid onset in disease occurrence world wide. Although the insulin resistance syndrome is viewed by the medical community as a defect of normal physiology, a plethora of available evidence indicates that the insulin resistant condition evolved among vertebrates as a survival strategy to enable increased survivability of ensuing, predictable seasons of low/no food (including glucose) availability.

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Introduction: Anthony Cincotta

I am a neuroendocrinologist by training, having received my Bachelor’s degree in biochemistry and molecular biology from the University of California, Santa Barbara and Master’s and Doctorate degrees from Louisiana State University (LSU) in physiology under the mentorship of Dr. Albert H. Meier. It was at LSU that my interest in the biological clock system and its role in the regulation of metabolic physiology was sparked by the revolutionary discoveries and elucidations made by Dr. Meier’s lab concerning biological clock mechanisms regulating physiology. He and his group in the early 1960s were the very first to demonstrate the existence in any organism of circadian rhythms of physiological responses to neuroendocrine factors. At LSU, I began investigating the possibility that modern human pathology of the metabolic syndrome (and several other progressive pathologies) was not a result of any “genetic defect” but of an environmentally induced (e.g., diet, stress, sleep-wake architecture) alteration of circadian neuroendocrine information presented to the clock system that then responded to direct the body to the obese/insulin resistant state as a survival response to such information.

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