I am excited to be a part of an innovative study that’s giving my team at the University of Chicago a fascinating glimpse into the relationship between insulin, sleep and body fat. We’ve been studying small biopsies of abdominal fat from volunteers who have taken part in sleep deprivation studies and are finding that when you’re sleep-deprived, you’re more likely to experience insulin resistance. This means that after you eat a meal, your body has to produce higher-than normal levels of insulin to handle the blood glucose levels in your bloodstream.
I’m collaborating on the study with Eve Van Cauter, PhD, and David Ehrmann, MD, internationally recognized researchers from the University of Chicago. Ehrmann is known for his studies on polycystic ovary syndrome, while Van Cauter conducted a range of widely published research that revealed an association between sleep deprivation and higher levels of body fat.
Normally, when insulin is released into the body, it releases a chemical that signals body cells – primarily in muscle, liver and fat tissue – to absorb glucose from the bloodstream. This process is known as insulin signaling. We’ve found that in sleep-deprived individuals, the insulin signaling process somehow goes awry, specifically at the site of fat cells.
Fat is actually your friend, but this fact gets lost sometimes in the literature. The adipose (fat) tissues are here to help you out. They’re a repository for long-term energy storage in the body. When adipose tissues can’t “do their job” and absorb blood glucose, the body senses that its own fat cells are starved for energy. It begins to resist weight loss, slowing its metabolism to conserve energy. The brain then produces chemicals leading to cravings for high-calorie foods.
Over time, insulin resistance also progresses into diabetes and heart disease, and it’s a known risk factor for breast cancer, pancreatic cancer, lymphoma, dementia, kidney disease, nerve damage and heart attack. Why sleep deprivation causes a “short” in insulin signaling remains a mystery. While the immediate solution may be obvious – get more sleep – some individuals struggle with chronic sleep disturbances, such as periodic limb movement disorder, which leads to wakefulness throughout the night. The problems can last for years despite attempts at treatment.
I’m studying the effects of various medications on insulin-resistant individuals, in hopes of finding a drug that restores the normal insulin signaling process. We’re also looking at the effects of bariatric surgery on insulin signaling. The procedure is a drastic intervention, and somewhat of a ‘last resort’ in morbidly obese people. But we know that one to two weeks after the surgery, there’s a marked improvement in the patient’s metabolic health. A lot of patients will go off their diabetes medications, including insulin, because their own insulin levels have returned to normal. The question is, how does insulin signaling change after the surgery? At this time, that’s completely unknown.
But the studies promise to shed new light on insulin signaling at the molecular level. The insulin signaling study crosses traditional boundaries of what we think of as sleep science or clinical science. It’s an exciting new frontier, and it’s been a privilege to collaborate with Dr. Van Cauter and Dr. Ehrmann.
Matthew Brady, PhD
Associate Professor of Medicine in the Section of Adult and Pediatric Endocrinology, Diabetes and Metabolism
The University of Chicago Medicine
Dr. Brady is a published researcher widely known for his studies on metabolism, insulin and obesity. If you’re interested in being involved in a sleep study, have type 2 diabetes and are 18 years of age or older, please call the University of Chicago at 773-795-0141 for more information. This article originally appeared in the fall issue of Kovler Connection. Click here to read the newsletter in its entirity.