Adipose tissue is a connective tissue that is composed of adipocytes (fat cells). It is divided into two forms – white adipose tissue and brown adipose tissue – with different functions. White adipose tissue has the following functions:
- Storage or depot fat – lipid stores (triglycerides); reserves to manage up to 40 days without food intake.
- Building fat – is mobilized as the last reserve in the event of food shortage.
- Isolating fat – In the subcutis is about 65% of the total fat, the rest is in the abdomen.
- Metabolic organ: metabolically active endocrine organ that secretes more than 600 bioactive molecules.
On the subject of adipose tissue and aromatase, see below “Female sex hormones“. The brown adipose tissue (plurivacuolar adipose tissue) is able to produce heat through the numerous content of mitochondria (“power plants of the cells”), by oxidation of fatty acids (shiver-free thermogenesis). This makes brown adipose tissue an “energy guzzler” compared to white fat. Approximately three quarters of fat consists of brown fat. Thermogenesis in brown adipose tissue is activated not only by cold, but also by eating. When eating, heat production increases due to oxidation of fatty acids. Research shows that shiver-free thermogenesis is also the prerequisite for the feeling of satiety to set in in the brain. The gene for the secretin receptor is also expressed in brown adipose tissue. When this receptor in brown adipose tissue is stimulated with secretin, immediate activation of shiver-free thermogenesis can be observed. Secretin release during eating first activates thermogenesis in brown fat and then leads to heating in the brain, which increases the feeling of satiety. Thus, food-induced thermogenesis consumes energy in brown fat and at the same time makes you feel full. Note: Statins (cholesterol-lowering drugs) reduce brown fat formation. Positron-emission tomography images demonstrated that patients who did not take statins had 6% brown adipose tissue; in contrast, patients who took statins had only 1% brown adipose tissue.
Adipocytes
Adipocytes secrete the following mediators:
- Adiponectins
- Adiponectin
- Apelin
- Leptin
- Lipocalin
- Omentin
- “Retinol-binding protein 4”
- Vaspin
- Visfatin/nicotinamide phosphoribosyltransferase
- Endocannabinoids and other lipids.
- Free fatty acids (FFS)
- Anandamide
- 2-arachidonylglycerol
- Enzymes
- Dipeptidyl peptidase 4
- Complement factors and similar substances
- Adipsin complement factor B
- “Scylating simulation protein”
- “C1q/TNF-related proteins”
- Lipid transport
- Apolipoprotein E
- “Cholesterol ester transfer protein”
- Lipoprotein lipase
- Prostaglandins
- Proteins of the fibrinolytic system
- Plasminogen activator inhibitor I (PAI 1).
- Proteins of the renin-angiotensin system.
- Angiotensinogen
- Angiotensin II
- Cytokines
- Tumor necrosis factor (TNF-alpha)
- Interleukin-6, -10, -18
- “Monocyte chemotactic protein 1”
- Resistin
- Progranulin
Only a small selection of mediators is briefly presented below:
Adiponectin
Adiponectin, a fat cell hormone, increases insulin sensitivity in muscle, facilitating the uptake and utilization of fatty acids (fatty acid oxidation). Furthermore, adiponectin has an anti-inflammatory effect (anti-inflammatory).obese patients have lowered adiponectin concentrations. This leads to inhibition of fatty acid oxidation and is associated with insulin resistance (decreased response of body cells to the hormone insulin) and metabolic syndrome, as well as atherosclerosis.
Angiotensin II
Angiotensin II has a potent vasoconstrictor (vasoconstricting) effect and promotes the formation of aldosterone – a mineralocorticoid – leading to sodium and water retention. Furthermore, angiotensin II promotes oxidative stress, activates the sympathetic nervous system (release of norepinephrine), and thus leads to hypertension (high blood pressure). See also “Renin-angiotensin-aldosterone system (RAAS)”.
Chemerin
Chemerin is mainly produced in adipose tissue and in the liver, kidneys, and pancreas. Among other things, it has an influence on the regulation of adipogenesis (the formation of fat cells) and chemotaxis (the release or formation of messenger substances (chemokines) that lead to the attraction of cells of the immune system (e.g., leukocytes) to the site of an inflammatory reaction). Chemerin is elevated even before the onset of myocardial infarction (heart attack) and apoplexy (stroke). As a signaling protein, it could be used in the future as an indicator to predict the risk of cardiovascular disease.
Fetuin-A
Fetuin-A has antiinflammatory effects, leading to lipid-induced inflammation (inflammation) and insulin resistance.
Interleukin-6
This mediator has an essentially proinflammatory (“proinflammatory”) effect.
Leptin
The anorexigenic (appetite-suppressing) hormone leptin is thought to be released by the rise in insulin after a meal: Leptin signals the food intake that has taken place, thereby stimulating the release of serotonin, among other things, and triggering the feeling of satiety. This explains why a defective leptin signal chain – for example due to insufficient secretion of leptin or a defective leptin receptor (leptin resistance) – leads to obesity. Furthermore, leptin has an influence on the following functions, among others: Basal metabolic rate, fertility, atherogenesis, and growth.
Plasminogen activator inhibitor (PAL 1)
Increased secretion of plasminogen activator inhibitor I (PAI 1) can lead to coagulation disorders and, consequently, thromboembolism.
“Retinol-binding protein 4” (RBP4)
RBP4 is associated with insulin resistance and visceral fat (abdominal fat) accumulation.
Tumor necrosis factor (TNF-alpha), IL-6, and other cytokines
Tumor necrosis factor-alpha (TNF-α, TNF alpha) essentially leads to proinflammatory processes.Increased secretion of TNF-alpha, IL-6, and other cytokines leads to insulin resistance, type 2 diabetes mellitus, chronic inflammation, and, consequently, atherosclerosis.
Vaspin
Vaspin causes hyperglycemia (high blood sugar) and reduces food intake. Further notes
- Hip fat does not increase the risk of cardiometabolic disease, unlike abdominal fat (waist-hip circumference increased/central obesity). Genetic variants that increase body mass index (BMI) but decrease waist-to-hip ratio actually result in a lower risk of disease (80% lower risk of cardiometabolic disease).
- Bacteria (mainly Proteobacteria and Firmicutes) and bacterial DNA in adipose tissue: these are associated with inflammation in obese and type 2 diabetic patients and appear to have an important role in initiating and maintaining local subclinical inflammation of adipose tissue. Interestingly in this context, patients on statin therapy have statistically fewer signs of inflammation than would have been expected based on their obesity.
