Insulin response? Huh? It’s just what it says, the way the body responds to insulin and the challenges that excite it in the first place. Insulin, as you recall, is a polypeptide hormone secreted by the islets of Langerhans in the pancreas. (A polypeptide, by the way, is made of two or more amino acids and becomes part of a protein.) Its job is to regulate metabolism of carbohydrates and fats, especially the conversion of glucose to glycogen, which lowers blood glucose levels. Glycogen is the chief carbohydrate storage material in animals, tucked nicely away mostly in the liver and partly in muscle, and can be liberated on demand. With insulin resistance the cells become less sensitive to the effects of insulin. If this happens, the pancreas is provoked to work harder and to release more of the hormone. Thus far, no disease is recognized, only a state wherein the body fails to respond. Sensitivity to insulin is widely different within the general population, so much so that the most insulin-sensitive people might be six times more so than those identified as most resistant. The prevalence of insulin resistance in the United States is about a fourth of the general population.
The most common condition related to insulin resistance is obesity, now a public health concern in its own right and a risk factor for type 2 diabetes, hypertension, and coronary artery disease. Losing weight increases the body’s sensitivity to insulin. Just a ten percent drop in weight can make a big difference. Of course, exercise enters the picture because it encourages the muscles to use glucose and gets rid of the spare tire. A high-fiber diet reduces levels of blood insulin and lowers risk of developing high blood pressure. Then there are drugs, decidedly the last resort. But there is now another factor that enters the scene, one to which we pay too little attention and take for granted—sleep, that marvelous cyclical event that restores body, mind and spirit.
A very recent study announced that fat cells need sleep as much as the cells in the brain. Lack of sleep and limited sleep have a direct and harmful effect on fat, a state that could lead to major health issues, including obesity and type 2 diabetes by increasing risk for insulin resistance. Under conditions controlled for calorie intake and physical activity, subjects in a cross-over study (where they change places after an allotted time) were allowed 4.5 or 8.5 hours of sleep. Insulin response in the fat cells was measured afterward. It was found that response to insulin after sleep restriction was 30% lower, dropping fat cell function to that of an obese or diabetic person, despite being physically fit (Broussard, 2012). Because many of us are sleep deprived, this is a significant finding, portending obesity, diabetes and other metabolic concerns.
Fat, or adipose tissue, serves an important function as an energy depot, and also prevents body heat loss and provides an elastic padding between organs. Having a density of about 0.9 kilogram per liter compared to muscle’s 1.06 kg/L, fat will float quite easily. Weight loss does not automatically make fat cells disappear; they merely shrink, waiting to balloon again under the right conditions. Fat may even become an active organ that sends chemical signals to other parts of the body, possibly triggering sickness and disease (ACS, 2010). Two of those signalers are leptin, which controls appetite, and adiponectin, a protein hormone that regulates glucose and fatty acid catabolism.
A single night of sleep deprivation may evoke hepatic insulin resistance and decrease glucose disposal rate, thereby affecting peripheral insulin sensitivity and disturbing more than one metabolic pathway (Donga, 2010). This upset of energy balance likewise presages disease manifestations that include thyroid dysregulation and weight gain (Bosy-Westphal, 2008). Where does weight gain fit in here? It seems that sleep deprivation stimulates the activity of ghrelin, a hormone produced by stomach cells that turns hunger on. Leptin is its counterpart. A French analysis of sleep-deprived men noted their consumption of as much as twenty-two percent more calories on the day after sleep restriction than they did with ample sleep (Brondel, 2010). These reports demonstrate a link between sleep loss and risk for chronic disorders (Chamorro, 2011).
The feverish pitch of world citizenship compromises our sleeping hours. Instead of the eight we need, many of us are lucky to see five or six. What used to be a complaint of college students has become a contagion that affects an increasing number of us. Medications and defined sleep disorders aside, the time for sleep needs to be assigned and followed, lest we open the door to the unwelcomed guests that accompany deprivation. One of the simplest steps to restore the time for sleep is to learn to say “no” so you can eliminate the other gremlins of sleep loss that include acne, insomnia and a sensitive stomach. If work worries keep you awake at night, look for ways to stop taking a fortune out of your bank of well-being, since renegade glucose metabolism is not a sweet deal.
ACS News Service Weekly PressPac: October 13, 2010 New evidence that fat cells are not just dormant storage depots for calories
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Sebastian M Schmid, Manfred Hallschmid, Kamila Jauch-Chara, Britta Wilms, Hendrik Lehnert, Jan Born, Bernd Schultes Disturbed glucoregulatory response to food intake after moderate sleep restriction. Sleep (impact factor: 5.05). 01/2011; 34(3):371-7.
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