Strictly speaking, we need to break down sleep into two dimensions:

It is a sleep duration disorder, the most typical of which is staying up late, insomnia, and being forced to wake up early.

They are sleep quality disorders, such as snoring (apnea), awakening, light sleep, sleepwalking, etc. In short, they are symptoms that interfere with quality.

Let’s talk about lack of sleep first

There has been a lot of research pointing to the fact that lack of sleep can lead to disorders of adipose cytokine secretion.

Why does obesity occur? The pathological basis is an increase in the number and size of fat cells. Fat in our body can be regarded as a huge organization composed of different departments and different positions. Fat storage is only half of the mission of this organization, and the other half is to play the role of the endocrine system.

Adipose tissue secretes many biologically active substances called [adipocytokines] through endocrine, paracrine, autocrine and other modes of action, some of which are specifically secreted (let’s think of them as Avengers), typically such as leptin, adipocytokine Vitamin, visfatin.

These cytokines play an important regulatory role in the occurrence and development of obesity. Under normal circumstances, adipocytokines will fulfill their duties, metabolize when excessive, store when appropriate, and release when insufficient, thereby ensuring a dynamic balance.

【Leptin】

It is a peptide hormone specifically secreted by adipose tissue. It is a 45 kb mRNA protein encoded by the obesity gene (Obese, Ob) and expressed in adipose tissue. It contains 146 amino acids and has the characteristics of a secreted protein. Its main function is to regulate the intake of sugar, fat and energy, prompt the body to reduce food intake, increase energy release, and inhibit the synthesis of fat cells, thereby reducing body weight.

But when there is insufficient sleep time, leptin will surge, and the increase in leptin will trigger their resistance. [1][2] To put it simply, when there are more people and the trade union organization becomes stronger, there will be strikes from time to time.

The result of leptin resistance is “You can eat as much as you want. Don’t worry, I won’t stop you from eating all the calories. I will use them all to synthesize fat.”

【Adiponectin】

Adiponectin is a peptide hormone composed of 244 amino acids, which inhibits inflammatory responses and regulates insulin sensitivity.

Insulin sensitivity is all too familiar. If blood sugar is too high, insulin will lower blood sugar. After all, high blood sugar is very close to fat synthesis.

Lack of sleep significantly reduces adiponectin levels, making insulin less sensitive. [3][4] Anyway, when you consume too much sugar, insulin is already very tired, and without anyone reminding it, it becomes more likely to paralyze itself.

*Other cytokines will not be introduced further.

Summary: Mechanistically speaking, lack of sleep will make those adipokine factors with specific functions ineffective and lose their ability to regulate fat. Cytokines also need time to repair themselves. Just working without rest is not enough.

Let’s talk about sleep disorders

Some people sleep for a long time, but the quality is not high, which still affects the increase of fat.

Take snoring, for example, the most common but most ignored symptom. In fact, persistent snoring should be called [sleep apnea syndrome].

When you snore while sleeping, your breathing is actually stopped. The longer you snore, the longer you hold your breath. This problem is huge: Let’s not talk about the various harms caused by hypoxia to the human body.

Intermittent hypoxia can lead to pancreatic β-cell dysfunction and insulin resistance in liver, skeletal muscle and adipose tissue, induce the differentiation of visceral adipose tissue macrophages into M1-pro-inflammatory subtype, upregulate and secrete many pro-inflammatory adipokines, and affect Insulin signaling pathway aggravates adipose tissue dysfunction. [5]

It is insulin resistance and the function of adipose tissue is impaired. Excess sugar can safely synthesize fat without hindrance.

Hypoxia also causes changes in NES-1 levels. NES-1 is a polypeptide, the product of the nuclear binding-2 peptide (NUCB2) gene, which can be expressed in the central nervous system, pituitary gland, stomach, pancreas, subcutaneous adipose tissue, etc. Its function is very direct: it suppresses appetite. However, in a long-term hypoxic environment, NES-1 levels will decrease, and appetite cannot be suppressed. [6][7]

So why do some people always think that fat people are more likely to snore? The truth may be very sad: some people suffer from long-term lack of oxygen due to snoring, so they eat and eat, so that snoring causes work-related injuries.

In short, in sleep medicine, sleep disorders need to be treated, because it seems to cause weight gain, and it can also cause various metabolic disorders and chronic diseases in invisible places.

Summary: Typical sleep disorders such as snoring start from hypoxia, causing glucose metabolism disorders, insulin resistance, and cytokine failure. In short, it is running all the way towards the destination of fat synthesis.

Summarize:

Lack of sleep can cause the failure of specific cytokines that regulate fat synthesis.

Poor sleep quality can cause metabolic abnormalities, insulin resistance, and cytokine failure.

In short, not only will the normal intake of calories accelerate cell synthesis, but it will also make you want to eat more.

references：

1. Considine RV, Sinha MK, Heiman ML. et a1． Semm immunoreactive. 1. ptin concentrations in normal—weight and obese humans[J]. NE “glJ Med, 1996, 334(5): 292-295.
2. Spi. geI K, Tasali E, Penev P, et a1. Sle. p curtailment in healthy you”g men is associated with decreased leptin levels, elevated ghrelin leVels, and increased hunger and 8ppetite[J]. Ann Intern Med, 2004, 141(11): 846-850.
3. Wang Suijun, Jia Weiping, Bao Yuqian, etc. The relationship between serum adiponectin and obesity[J]. Chinese Journal of Endocrinology and Metabolism, 2005, 2l(1): 36-38.
4. jmpson Ns, Banks s, Armyo s, et a1. Effects of sleep restriction on adiponectin leVels jn healthy men and women[J]． Physiol Behav, 2010, 101(5): 693-698.
5. RYAN S. Adipose tissue inflammation by intermittent hypoxia: mechanistic link between obstructive sleep apnoea and metabolic dysfunction［J］. J Physiol, 2017, 595(8): 2423-2430.
6. AYADA C, TORU Ü, KORKUT Y. Nesfatin – 1 and its effects on different systems［J］. Hippokratia, 2015, 19(1): 4-10.
7. Wang Yu, Xie Xin, Bai Jinxiu, et al. Changes and significance of serum ghrelin and feeding inhibitory factor 1 levels in children with dwarfism before and after growth hormone treatment [J]. Journal of Practical Medicine, 2019, 35 (19): 3038-3041.