Type 2 Diabetes

In this week's Homerun Slides, the approach that shows how earlier and more aggressive type 2 diabetes intervention may improve a patient's chance to reach management goals.

In this week's Homerun Slides, the effect of GLP-1 within the human system.

Semaglutide reduced major cardiovascular events by 26% in adults with type 2 at high cardiovascular risk.

For those healthcare providers who treat diabetes with any kind of regularity, it has become increasingly obvious that several of our patients fall outside the current diabetes classification system. With individualization of patient care being the new focus, it can be challenging to accomplish this, when certain diabetic individuals don’t “conform” to the current definitions.

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

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.

Are clinicians intensifying treatment before it is too late?