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.

The development of type 2 diabetes is multifactorial. All of the following are thought to play a role in the development EXCEPT: 1. Genetics 2. Environmental factors 3. Elevated circulating free fatty acid levels 4. Pancreatic α-cell defects 5. Increased skeletal GLUT4 glucose transporters translocation capacity Did you get it right? Follow the link to find out!

Friend of Diabetes in Control and frequent guest author David Kliff, Diabetic Investor, shared his views on some of the news coming out of EASD. As always, his ideas are thought-provoking. We reached out to some of our Advisory Board members to get their responses to David’s piece, and they provided additional strong viewpoints for your consideration.

What should be the proper treatment selection for patients with type 2 diabetes?

Scientists believe drug commonly prescribed for T2 could be routinely taken by T1 patients.

What benefits can lixisenatide provide when added to basal insulin regimen?

Empagliflozin might not only decrease the risk of cardiovascular events in patients with type 2, but also renal events.