Sleep and metabolism

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Sleep is important in regulating metabolism. Mammalian sleep can be sub-divided into two distinct phases - REM (rapid eye movement) and non-REM (NREM) sleep. In humans and cats, NREM sleep has four stages, where the third and fourth stages are considered slow-wave sleep (SWS). SWS is considered deep sleep, when metabolism is least active. [1]

Contents

Metabolism involves two biochemical processes that occur in living organisms. The first is anabolism, which refers to the build up of molecules. The second is catabolism, the breakdown of molecules. These two processes work to regulate the amount of energy the body uses to maintain itself. During non-REM sleep, metabolic rate and brain temperature are lowered to deal with damages that may have occurred during time of wakefulness. [1]

Normal metabolism

After eating, the pancreas releases insulin. Insulin signals muscle and fat cells to absorb glucose from food. As a result, blood glucose levels return to normal. [2]

Sleep loss and Type 2 diabetes

Insulin-Resistant Metabolism

Several studies suggest that the association between sleep loss, obesity, and diabetes risk, may be driven by several factors. Three main examples are altered glucose metabolism, increased appetite, and lower energy expenditure. [3]

Baseline levels of insulin do not signal muscle and fat cells to absorb glucose. When glucose levels are elevated, the pancreas responds by releasing insulin. Blood sugar will then rapidly drop. This can progress to type 2 diabetes. [2] Sleep variations, both in quantity and quality, may affect metabolic regulation in type 2 diabetes. Additional data has shown a correlation between sleep quality and type 2 diabetes risk. [4]

Sleep loss can affect the basic metabolic functions of storing carbohydrates and regulating hormones. Reduction of sleep from eight hours to four hours produces changes in glucose tolerance and endocrine function. Researchers from the University of Chicago Medical Center followed 11 healthy young men for 16 consecutive nights. The first 3 nights, the young men slept for the normal 8 hours. The next 6 nights, they slept for 4 hours. The next 7 nights, they spent 12 hours in bed. They all had the same diet. They found that there were changes in glucose metabolism that resemble that of type 2 diabetes patients. When the participants were tested after sleep deprivation, they took 40% longer than normal to regulate blood sugar levels after a high-carbohydrate meal. The secretion of insulin and the body's response to insulin decrease by 30%. Sleep deprivation also alters the productions of hormones, lowering the secretion of thyroid stimulating hormone and increasing blood levels of cortisol. [5] [ medical citation needed ] Increased cortisol levels in turn induce insulin resistance, resulting in raised blood glucose. [4]

It has also been shown that when slow-wave sleep was suppressed for three nights, young healthy subjects were 25% less sensitive to insulin. [3] They needed more insulin to get rid of the same amount of glucose. If the body does not release more insulin to compensate, the blood-glucose levels will increase. This resembles impaired glucose tolerance, which can result in type 2 diabetes. [5] [6] [ medical citation needed ]

Sleep loss and appetite control

Sleep plays a vital role in regulating metabolism and appetite. When sleep deprived, the metabolic system will be out of balance, which will ultimately affect the dietary choices people make. Teens who are sleep deprived crave more carbohydrates. Sleep deprivation is a risk factor for obesity among young adults. [7] [ medical citation needed ]

There are two hormones, leptin and ghrelin, that are important in appetite control. Leptin, released by adipose tissue, is a hormone that inhibits appetite and increases energy expenditure. Ghrelin, released from the stomach, is a hormone that increases appetite and reduces energy expenditure. In a study where subjects were restricted to 4 hours of sleep per night for 2 nights, leptin levels decreased by 18% and ghrelin levels increased by 28%. In addition, there was an increase in hunger rating by 23%, with leptin levels being a significant predictor of hunger levels. Subjects also preferred high carbohydrate foods (sweets, salty food and starchy food), and craving for salty food increased by 45%. Sleep deprivation may cause people to intake food for emotional/psychological need rather than caloric need of the body. [1] [2]

Sleep loss and obesity

Chronic sleep deprivation (less than 8 hours of sleep) is associated with an increase in body mass index (BMI) and obesity. In a study with 3000 patients, it was found that men and women who sleep less than 5 hours have elevated body mass index (BMI). In another study that followed about 70.000 women for 16 years, there was a significant increase in body weight in those who slept 5 hours or less compared to those who slept 7–8 hours. [1] [2] [8]

As sleep time decreased over time from the 1950s to 2000s from about 8.5 hours to 6.5 hours, there has been an increase in the prevalence of obesity from about 10% to about 23%. [2]

Weight gain itself may also lead to a lack of sleep as obesity can negatively affect quality of sleep, as well as increase risk of sleeping disorders such as sleep apnea. [9] [10]

Sleep loss and skeletal muscle metabolism

Sleep loss also affects the metabolism of skeletal muscle. Insufficient sleep has been shown to decrease myofibrillar and sarcoplasmic muscle protein synthesis and contribute to the development of muscle atrophy. [11]

Studies have also shown that detrimental effects on muscle protein synthesis caused by sleep loss can be mitigated by exercise. [11]

Related Research Articles

<span class="mw-page-title-main">Hypoglycemia</span> Health condition

Hypoglycemia, also called low blood sugar, is a fall in blood sugar to levels below normal, typically below 70 mg/dL (3.9 mmol/L). Whipple's triad is used to properly identify hypoglycemic episodes. It is defined as blood glucose below 70 mg/dL (3.9 mmol/L), symptoms associated with hypoglycemia, and resolution of symptoms when blood sugar returns to normal. Hypoglycemia may result in headache, tiredness, clumsiness, trouble talking, confusion, fast heart rate, sweating, shakiness, nervousness, hunger, loss of consciousness, seizures, or death. Symptoms typically come on quickly.

Insulin resistance (IR) is a pathological condition in which cells either fail to respond normally to the hormone insulin or downregulate insulin receptors in response to hyperinsulinemia.

<span class="mw-page-title-main">Type 2 diabetes</span> Form of diabetes mellitus

Type 2 diabetes (T2D), formerly known as adult-onset diabetes, is a form of diabetes mellitus that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. Common symptoms include increased thirst, frequent urination, fatigue and unexplained weight loss. Symptoms may also include increased hunger, having a sensation of pins and needles, and sores (wounds) that do not heal. Often symptoms come on slowly. Long-term complications from high blood sugar include heart disease, stroke, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations. The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon.

<span class="mw-page-title-main">Leptin</span> Hormone that inhibits hunger

Leptin also obese protein is a protein hormone predominantly made by adipocytes. Its primary role is likely to regulate long-term energy balance.

<span class="mw-page-title-main">Appetite</span> Desire to eat food

Appetite is the desire to eat food items, usually due to hunger. Appealing foods can stimulate appetite even when hunger is absent, although appetite can be greatly reduced by satiety. Appetite exists in all higher life-forms, and serves to regulate adequate energy intake to maintain metabolic needs. It is regulated by a close interplay between the digestive tract, adipose tissue and the brain. Appetite has a relationship with every individual's behavior. Appetitive behaviour also known as approach behaviour, and consummatory behaviour, are the only processes that involve energy intake, whereas all other behaviours affect the release of energy. When stressed, appetite levels may increase and result in an increase of food intake. Decreased desire to eat is termed anorexia, while polyphagia is increased eating. Dysregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

<span class="mw-page-title-main">Sleep debt</span> Cumulative effect of not getting enough sleep

Sleep debt or sleep deficit is the cumulative effect of not getting enough sleep. A large sleep debt may lead to mental or physical fatigue, and can adversely affect one's mood, energy, and ability to think clearly.

<span class="mw-page-title-main">Adiponectin</span> Mammalian protein found in Homo sapiens

Adiponectin is a protein hormone and adipokine, which is involved in regulating glucose levels and fatty acid breakdown. In humans, it is encoded by the ADIPOQ gene and is produced primarily in adipose tissue, but also in muscle and even in the brain.

<span class="mw-page-title-main">Ghrelin</span> Peptide hormone involved in appetite regulation

Ghrelin is a hormone primarily produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, and is often called a "hunger hormone" because it increases the drive to eat. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility and stimulating the secretion of gastric acid.

<span class="mw-page-title-main">Weight gain</span> Increase in a persons total body mass

Weight gain is an increase in body weight. This can involve an increase in muscle mass, fat deposits, excess fluids such as water or other factors. Weight gain can be a symptom of a serious medical condition.

<span class="mw-page-title-main">Hyperinsulinemia</span> Abnormal increase in insulin in the bloodstream relative to glucose

Hyperinsulinemia is a condition in which there are excess levels of insulin circulating in the blood relative to the level of glucose. While it is often mistaken for diabetes or hyperglycaemia, hyperinsulinemia can result from a variety of metabolic diseases and conditions, as well as non-nutritive sugars in the diet. While hyperinsulinemia is often seen in people with early stage type 2 diabetes mellitus, it is not the cause of the condition and is only one symptom of the disease. Type 1 diabetes only occurs when pancreatic beta-cell function is impaired. Hyperinsulinemia can be seen in a variety of conditions including diabetes mellitus type 2, in neonates and in drug-induced hyperinsulinemia. It can also occur in congenital hyperinsulinism, including nesidioblastosis.

<span class="mw-page-title-main">Reactive hypoglycemia</span> Medical condition

Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within four hours after a high carbohydrate meal in people with and without diabetes. The term is not necessarily a diagnosis since it requires an evaluation to determine the cause of the hypoglycemia.

Nesfatin-1 is a neuropeptide produced in the hypothalamus of mammals. It participates in the regulation of hunger and fat storage. Increased nesfatin-1 in the hypothalamus contributes to diminished hunger, a 'sense of fullness', and a potential loss of body fat and weight.

<span class="mw-page-title-main">Blood sugar regulation</span> Hormones regulating blood sugar levels

Blood sugar regulation is the process by which the levels of blood sugar, the common name for glucose dissolved in blood plasma, are maintained by the body within a narrow range.

<span class="mw-page-title-main">Equine metabolic syndrome</span> Endocrinopathy affecting horses and ponies

Equine metabolic syndrome (EMS) is an endocrinopathy affecting horses and ponies. It is of primary concern due to its link to obesity, insulin dysregulation, and subsequent laminitis. There are some similarities in clinical signs between EMS and pituitary pars intermedia dysfunction, also known as PPID or Cushing's disease, and some equines may develop both, but they are not the same condition, having different causes and different treatment.

Hunger is a sensation that motivates the consumption of food. The sensation of hunger typically manifests after only a few hours without eating and is generally considered to be unpleasant. Satiety occurs between 5 and 20 minutes after eating. There are several theories about how the feeling of hunger arises. The desire to eat food, or appetite, is another sensation experienced with regard to eating.

Ingestive behaviors encompass all eating and drinking behaviors. These actions are influenced by physiological regulatory mechanisms; these mechanisms exist to control and establish homeostasis within the human body. Disruptions in these ingestive regulatory mechanisms can result in eating disorders such as obesity, anorexia, and bulimia.

<span class="mw-page-title-main">Sympathoadrenal system</span>

The sympathoadrenal system is a physiological connection between the sympathetic nervous system and the adrenal medulla and is crucial in an organism's physiological response to outside stimuli. When the body receives sensory information, the sympathetic nervous system sends a signal to preganglionic nerve fibers, which activate the adrenal medulla through acetylcholine. Once activated, norepinephrine and epinephrine are released directly into the blood by adrenomedullary cells where they act as the bodily mechanism for "fight-or-flight" responses. Because of this, the sympathoadrenal system plays a large role in maintaining glucose levels, sodium levels, blood pressure, and various other metabolic pathways that couple with bodily responses to the environment. During numerous diseased states, such as hypoglycemia or even stress, the body's metabolic processes are skewed. The sympathoadrenal system works to return the body to homeostasis through the activation or inactivation of the adrenal gland. However, more severe disorders of the sympathoadrenal system such as pheochromocytoma can affect the body's ability to maintain a homeostatic state. In these cases, curative agents such as adrenergic agonists and antagonists are used to modify epinephrine and norepinephrine levels released by the adrenal medulla.

Sleep and weight is the association between the amount of sleep an individual obtains and the weight of that individual.

Obesity is defined as an abnormal accumulation of body fat, usually 20% or more over an individual's ideal body weight. This is often described as a body mass index (BMI) over 30. However, BMI does not account for whether the excess weight is fat or muscle, and is not a measure of body composition. For most people, however, BMI is an indication used worldwide to estimate nutritional status. Obesity is usually the result of consuming more calories than the body needs and not expending that energy by doing exercise. There are genetic causes and hormonal disorders that cause people to gain significant amounts of weight but this is rare. People in the obese category are much more likely to suffer from fertility problems than people of normal healthy weight.

<span class="mw-page-title-main">Pathophysiology of obesity</span> Physiological processes in obese people

Pathophysiology of obesity is the study of disordered physiological processes that cause, result from, or are otherwise associated with obesity. A number of possible pathophysiological mechanisms have been identified which may contribute in the development and maintenance of obesity.

References

  1. 1 2 3 4 Sharma, Sunil; Kavuru, Mani (2 August 2010). "Sleep and Metabolism: Overview". International Journal of Endocrinology. 2010: 1–12. doi: 10.1155/2010/270832 . PMC   2929498 . PMID   20811596.
  2. 1 2 3 4 5 Walker, Matthew (October 10, 2011). "Sleep Deprivation I: Immune Function and Metabolism".
  3. 1 2 Knutson, Kristen L.; Spiegel, Karine; Penev, Plamen; Van Cauter, Eve (June 2007). "The metabolic consequences of sleep deprivation". Sleep Medicine Reviews. 11 (3): 163–178. doi:10.1016/j.smrv.2007.01.002. PMC   1991337 . PMID   17442599.
  4. 1 2 Darraj, Ali (2023-11-03). "The Link Between Sleeping and Type 2 Diabetes: A Systematic Review". Cureus. 15 (11): e48228. doi: 10.7759/cureus.48228 . ISSN   2168-8184. PMC   10693913 . PMID   38050514.
  5. 1 2 "Lack of Deep Sleep May Increase Risk of Type 2 Diabetes". Science Daily. Retrieved November 30, 2011.
  6. ↑ "Sleep and Metabolism: An Overview".
  7. ↑ "Daytime Sleepiness is associated with an increased craving for carbs among teen". Science Daily. Retrieved November 30, 2011.
  8. ↑ Trebekk (2007). "Sleep and metabolic control: waking to a problem?". Clinical and Experimental Pharmacology and Physiology. 34 (1–2): 2–3.
  9. ↑ Fatima, Y.; Doi, S. A. R.; Mamun, A. A. (2016). "Sleep quality and obesity in young subjects: a meta-analysis" (PDF). Obesity Reviews. 17 (11): 1154–1166. doi:10.1111/obr.12444. ISSN   1467-7881. PMID   27417913.
  10. ↑ Strobel, Richard J.; Rosen, Raymond C. (1996). "Obesity and Weight Loss in Obstructive Sleep Apnea: A Critical Review". Sleep. 19 (2): 104–115. doi:10.1093/sleep/19.2.104. ISSN   1550-9109. PMID   8855032.
  11. 1 2 Morrison, Matthew; Halson, Shona L.; Weakley, Jonathon; Hawley, John A. (2022-12-01). "Sleep, circadian biology and skeletal muscle interactions: Implications for metabolic health" (PDF). Sleep Medicine Reviews. 66: 101700. doi:10.1016/j.smrv.2022.101700. ISSN   1087-0792. PMID   36272396.
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