There is (adipose); White Adipose Tissue (WAT), Brown Adipose Tissue (BAT).
White adipose tissue (BAT)
BYD releases the excess energy taken back into the bloodstream when necessary. It stores it as triglyceride (TG) to be secreted in the form of triglyceride (TG). White adipose tissue plays a role in lipid storage, hormone production, immune function and regional tissue structure. White adipose tissue is stored in 2 main regions in the body: visceral white adipose tissue (vBYD) and subcutaneous white adipose tissue (scBYD). Visceral BYD is adipose tissue surrounding the internal organs, while scBYD is found in the thighs and buttocks. Increased level of visceral fat in the body is associated with insulin resistance, type 2 diabetes, dyslipidemia, development of atherosclerosis, fatty liver and mortality.
Brown adipose tissue (BFA): Robert E Smith described the thermogenic capacity of CF in 1961. . After this identification, in 1978, it was found that UCP-1, the main component of KYD mitochondria, was responsible for regulating energy distribution.
Brown adipose tissue (BFA); Although it is less abundant in the body than BYD (White Fat Tissue), it produces heat through adaptive thermogenesis in response to cold and diet.
Brown adipose tissue; It is found in large amounts in small mammals and newborns, allowing them to survive in cold weather. It provides thermoregulation especially in mammals and newborns.
While it was thought for a long time that CFD did not occur in adults, it was later understood that adults also had metabolically active CFD and could play an important role in energy balance. Low body weight is associated with a high amount of brown adipose tissue in adult humans. Sympathetic nervous system activation in response to cold exposure and food intake causes stimulation of brown adipose tissue. This condition, centered on brown adipose tissue, is defined as cold-induced thermogenesis and the thermic effect of nutrients and increases total energy expenditure.
If we examine the differences between White Adipose Tissue and Brown Adipose Tissue;
White Adipose Tissue;
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The largest fat reservoir in humans is white adipose tissue.
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Midochondria in white adipocytes is weakened. It is low and variable in amount.
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It has been observed that the amount of mitochondrial DNA in white adipose tissue decreases in obese individuals.
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Impaired mitochondrial activity predisposes to obesity. It has been reported that mitochondrial biogenesis changes in obesity.
Brown adipose tissue;
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Many It contains small polygonal fat drops of variable diameter and multilocular adipocytes.
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Mitochondria, the most important organelle, are large, spherical and abundant.
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Since brown fat tissue needs more oxygen, it contains more capillaries than white fat tissue.
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In addition, the nerve supply is more intense in KYD than in BYD.
Uncoupling protein1 (UCP1), located in the inner mitochondrial membrane, is the determining protein of KYD and It allows it to be released as heat during consumption.
The color of brown adipose tissue is due to its large amount of mitochondria and high level of vascularity. Substrates for brown adipose tissue; Fatty acids coming from triglycerides in the tissue are free fatty acids and lipoproteins in the circulation.
In adipocytes, acetyl CoA is formed both from pyruvate produced from glucose by glycolysis and from fatty acids by b-oxidation. After the oxidation of acetyl groups in the creps ring, the final energy in BYD is ATP, while in KYD it is released as heat.
Brown adipose tissue is one of the current issues that attracts attention in the treatment of the components of metabolic syndrome. Some new theories have emerged with the discovery of the hormone called irisin, which is secreted by skeletal muscle and is linked to exercise.
Development of fatty tissues; Adipocytes (and myocytes) arise from the mesoderm. During fetal development, CYD occurs earlier than BYD. White adipose tissue begins to develop in mid-pregnancy and is at its largest size relative to body weight from birth. In humans, white fat cell stores gradually increase after birth.
It was previously thought that white and brown adipose tissue came from the same root. Look at the research done If it happens; Seale et al.; A study he conducted showed that brown fat cells and muscle cells derive from the same stem cell. Apart from their contractile properties, brown fat cells are similar to muscle cells. Muscle-like brown fat cells are stimulated by the sympathetic nervous system (CNS). Timmos et al.; showed that, unlike white fat cells, muscle and brown fat cells carry the myogenic factor 5 (Myf5+) marker.
DIFFERENTIATION OF ADIPOCITES
Browning of white adipose tissue is anatomically; White Adipose Tissue appears as Brown Adipose Tissue with thermogenic stimulation. Factors that cause White Fat Tissue to turn into Brown Fat Tissue; hormonal interactions, chronic cold exposure, exercise and environmental factors. The browning process can be mimicked by chronic treatment usingβ-adrenergic receptor activators.
If we examine the effect of age on fat tissues:
As age progresses; There is a decrease in Total Body Mass. The reflection of this decrease in body fat percentage; The fat percentage remains constant or decreases slightly. In a study examining the changes in the amount of CFD according to the stage of sexual development; In the pre-adolescent period (stage 1); It has been reported that the amount of KYD is significantly less and that there is a large increase in the amount of KYD in both girls and boys during the last two stages of adolescence. Compared to the adolescence period (stage 2-5) Brown Adipose Tissue function decreases with increasing age! Cold-induced CF activity; While it is more than 50% in the 20s, it is at lower levels in the 50-60s.
The decrease in thermoregulation generally results in a decrease in cold tolerance and deterioration in body weight control. The reason for the decrease in thermoregulation in older ages is; It can be said that it is more related to the atrophy of the KYD and the age-related decrease in its amount, rather than the decrease in the activation of KYD.
Location and Visualization of Fat Tissues in the Body
Adult humans KYD in moments; It is found distributed in the upper part of the cervical, supraclavicular, axillary, paravertebral and mediastinal abdominal region.
Body composition measurement techniques; bioelectrical impedance analysis, air displacement plethysmography, dual energy X-ray absorptiometry, MRI or magnetic resonance spectroscopy. In general, body total BMD and KYD, including visceral, subcutaneous and intramuscular, can be determined with body composition measurement techniques. To date, brown adipose tissue imaging studies performed with positron emission tomography-computed tomography (PET/CT) have been performed with fluorodeoxyglucose (FDG). Fluorodeoxyglucose is retained by metabolically active KYD. KYD depiction made with this method; It can be affected by many physiological and technical factors such as age, gender, body composition, FDG dose, season and temperature during operation. Recently, magnetic resonance imaging (MRI) and spectroscopy (MRS) are new methods that use.
Adipose Tissue as an Endocrine Organ
Adipose tissue secretes various hormones; It plays a role in the development of pathological conditions such as inflammation, insulin resistance, obesity and metabolic syndrome.
Adipocytes; It secretes polypeptides such as leptin, resistin and adiponectin.
LEPTIN; Leptin, found both in the circulation and in the cerebrospinal fluid, is secreted from adipocytes. Leptin production is higher in subcutaneous BYD than in visceral BYD. Large fat cells contain more leptin than small fat cells. While excessive energy intake, insulin and glucose levels increase leptin production; Hunger, cold, β-adrenergic agonists and testosterone cause a decrease in leptin levels. Leptin regulates energy homeostasis by activating the thermoregulatory response, especially CFD. Additionally, leptin induces weight loss through thermogenesis in CFD, independently of food intake.
RISE; Your iris; It is a newly discovered myokine isolated from muscle tissue for the first time. As a result of research, it has been seen that it is synthesized and released in many tissues, and its main source is stated to be skeletal muscle and fat tissue.
The structure of the irisin hormone; While it is 100% similar in humans and mice, insulin is 85% similar, glucagon is 90%, and leptin is 100% similar. e is 83%. There is a protein called coupling disrupting protein-1 (UCP-1) in the inner part of the mitochondrial membranes of the new tissue formed when irisin transforms white adipose tissue into brown adipose tissue.
Stimulated by exercise and cold. Irisin increases the expression of the UCP-1 pump in white adipose tissue cells.
White adipose tissue cells with increased UCP-1 pump in their mitochondria are called beige adipose tissue. These cells work like brown adipose tissue cells. Increased UCP-1 expression inhibits ATP synthesis and heat production, which causes energy consumption in the cell, increases, ensuring thermogenesis and glucose homeostasis. Another mechanism of action of irisin is through the receptor found in adipocytes. Iris binding to the receptor increases adenylate cyclase activity. Thus, the amount of cyclic adenosine monophosphate (cAMP) increases. Increased cAMP synthesis activates hormone sensitive lipase and protein kinase A. Thus, lipolysis and energy expenditure are increased.
Relationship of irisin with diseases
It is thought that it can prevent the onset of obesity and diabetes thanks to its relationship with glucose/lipid metabolism. Reduction in skeletal muscle volume is a factor in insulin resistance, and irisin is associated with insulin resistance to a greater extent than other myokines. However, a consensus has not yet been reached regarding the release of irisin from skeletal muscle
Relationship of irisin with obesity and diabetes
Many genetic and environmental factors such as diabetes and obesity play a role. It is a multifactorial disease, and it has been concluded that obesity makes it difficult to control diabetes and also has negative effects on glycemic control. In recent years, it has become an important issue that the interaction between fat tissue and muscle tissues plays a role in the regulation of body weight. A mechanism in which irisin secretion increases in response to decreased glucose/lipid metabolism has been reported in non-diabetic obese patients
Exogenous administration of irisin using adenoviral drug initiated a brown adipose tissue-like development program in certain depots of white adipose tissue and; increased energy expenditure, improved glucose tolerance and moderate
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