Woman, 64 years of age. History of Class II Obesity and hyperlipidemia. While she had obesity, her glucose levels were elevated. A1C 8.2%. She followed a lower carb meal plan, was active, took metformin and a GLP-1, a statin and an ACE-I. She lost 22% total body weight. A1C then remained in the 6-6.5% range for 3 years on this treatment plan. Over the past 8 months, due to insurance and her statement of denial that she ever really had diabetes, she stopped taking her glucose-lowering medication, statin, and ACE-I, wasn’t as strict with meal plan or activity, and stopped checking her glucose, but did not gain back her weight.

Dr. Yehuda Handelsman talks with Diabetes in Control Publisher Steve Freed at the 2016 AACE Meeting. In part 3 of this Exclusive Interview, Dr. Handelsman explains how he prioritizes medications/lifestyle changes when treating diabetes and managing various co-morbidities.

In this week's Homerun Slides, understanding the development and progression of type 2 diabetes.

Sympathetic effects and mediation: Sympathetic nerves inhibit insulin and stimulate glucagon secretion. Their activation may help mediate stress-induced changes in islet hormone secretion including the glucagon counterregulatory response to hypoglycemia.These effects may be mediated by the combination of the classical neurotransmitter noradrenaline and the sympathetic neuropeptides (galanin and NPY). All three neurotransmitters can inhibit insulin and stimulate glucagon secretion, thus mimicking the effects of sympathetic activation on islet hormone secretion. In addition, galanin and NPY meet several other of the criteria needed to be classified as a physiologic neurotransmitter.

In November of 2007 we ran a small article on the use of fast acting bromocriptine to reset the metabolic clock in patients with diabetes. This article caused us to receive a lot of questions on how the drug worked, and one of our PharmD candidates prepared a great article on …

In part 2 of this exclusive ADA interview, Anthony Cincotta discusses the Cycloset Safety Trial study design and findings regarding the cardiovascular safety of Cycloset.

In part 1 of this exclusive ADA interview, Anthony Cincotta discusses the mechanistic science behind the development of Cycloset, and why preclinical and clinical findings suggest the therapy may reset clock mechanisms governing postprandial glucose metabolism.

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.

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.

This week the take home message asks us to change from “start low and go slow,” to “be aggressive not repressive.” More and more documentation shows the value of adding newer classes of medications sooner to get our patients to target. Part of this comes from the sheer acknowledgement that …