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Deposition (storage) of fats.
There are two mechanisms for storing fat; capturing them (triacylglycerides) from plasma and lipogenesis is the synthesis of fats from other sources, in particular, glucose.
Adipose tissue - a kind of self-charging energy battery, it is constantly involved in the metabolism. In the condition of rest, after a meal, in fat cells (adipocytes) glucose is transformed into fatty acids and triglycerides with the accumulation of energy.
Fats (triacylglycerides) are in the blood in the form of lipoprotein particles. The largest of these particles (containing the highest amount of triacylglycerides) are too large to penetrate from the capillaries into the intercellular fluid, and from there into fat cells (adipocytes).
But there is a mechanism to overcome this difficulty. Fat cells (adipocytes) secrete one enzyme, lipoprotein lipase, which cleaves lipoprotein particles to free fatty acids, and they can already freely enter the intercellular fluid and reach adipocytes.
Once in the fat cells (adipocytes) fatty acids are collected in lipid droplets for accumulation in the cell.
Lipoprotein lipase activity in adipose tissue is regulated by what do you think ?! Insulin released in response to a rise in glucose concentration in the blood. Since we rarely eat pure fat, after a normal meal that contains both fats and carbohydrates, the absorption of fats into adipose tissue is stimulated by insulin. The effect of insulin on enzyme activity (lipoprotein lipase) is to enhance the secretion and activation of this enzyme by adipose tissue cells and its transport to the endothelium. This process takes 3-4 hours. At the same time in fatty tissue, esterification of fatty acids is also stimulated by insulin.
The main thing to be understood from this is that insulin stimulates both the uptake and the accumulation of fat circulating in the blood in adipose tissue.
Another possible mechanism for fat deposition is lipogenesis or the pentose phosphate pathway, also stimulated by insulin.
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Deposition (storage) of fats.
- Fatty infiltration and fatty degeneration
If the fats entering the cells do not split, do not oxidize, and are not removed from it, this indicates fatty infiltration. When combined, infiltration with a violation of the structure of the protoplasm and its protein component speak of fatty degeneration. A common cause of fatty infiltration and fatty degeneration is considered to be the suppression of the activity of oxidative and hydrolytic lipid metabolism enzymes (with
- Crystal deposition arthropathy
Intra-articular deposits of crystals are associated with many acute and chronic changes in the joints. Endogenous crystals that cause pathological changes are monosodium urate crystals (uric acid salts), calcium pyrophosphate dehydrate and basic calcium phosphate (hydroxyapatite). Exogenous crystals of esters of corticosteroids, talc, polyethylene and methyl methacrylate can also
- Fat embolism (traumatic). Other obstetric embolism. Obstetric Fat Embolism
Code on ICD-10 Fatty embolism (traumatic) T79.1 Other obstetric embolism. Obstetric fat embolism O88.8 Diagnosis When making a diagnosis Mandatory Anamnesis (trauma, childbirth, surgery with osteometallosynthesis, extensive burns, severe metabolic disorders, intravenous fat emulsions, closed heart massage, etc.), blood pressure, heart rate, BH, examination of the skin and mucous membranes (rash)
- Subcutaneous fat layer:
• the degree of development, the nature of the spread, the thickness of the subcutaneous fat fold in the abdomen, chest, back, limbs, face; • the presence of edema and seals; • tissue turgor. Some idea of the number and distribution of the subcutaneous fat layer can be obtained from a general examination of the child, but the final judgment on the state of the subcutaneous fat layer is made only after palpation. For
- Fat embolism
Fat embolism syndrome may develop from 1 hour to three days after injury. Although fat embolism is more often associated with a fracture of the tubular bones or pelvis, its causes have also been reported such as diabetes, fatty liver, pancreatitis, joint surgery, and sickle cell anemia. It is theoretically believed that lung damage develops when lipases hydrolyze neutral
- Fat absorption
Fats in food consist mainly of triglycerides, phospholipids (lecithin) and cholesterol (in the form of esters) (Fig. 6-17). For a complete digestion and absorption of fats, a combination of several factors is necessary: the normal functioning of the liver and biliary tract, the presence of pancreatic enzymes and alkaline pH, the normal state of the enterocytes, the intestinal lymphatic system and the functional
- FAT EMBOLES SYNDROME
Fatty embolus syndrome (FGD) is the clinically manifested systemic intravascular dissemination of neutral fat globules inside microvessels. Fat embolism - recognition of the fact of embolization, but without clinical manifestations. Etiopathogenesis. Most often, the SCF develops with fractures of the long tubular bones of the lower extremities, pelvic bones. The risk of developing the syndrome increases with
- Fat embolism
Symptoms of fat embolism: • ???? arterial hypoxemia (this symptom may be the only one); • ???? acute respiratory distress syndrome; • ????? dysfunction of the central nervous system (motor restlessness, coma, epi-attacks) • ???? petechiae (neck, forearm, chest); • coagulopathy;
- Liver fatty degeneration (steatosis)
Causes Excessive consumption of alcohol, fatty foods, overweight, diabetes mellitus, prolonged exposure to chemicals, solvents such as benzene, carbon tetrachloride, chloroform, effects of taking drugs like cortisone (or tetracycline). As a rule, after eliminating the cause, fatty deposits in the liver disappear. Severe malaise develops in cirrhosis of the liver. Next is
- DISTURBANCES OF FAT ACCUMULATION IN FATTY TISSUE. OBESITY
These disorders manifest themselves either in the form of exhaustion as an extreme version of weight loss, or in the form of obesity. Depletion (see "Disruption of protein metabolism") is observed with insufficient intake of calories from food in relation to energy needs. Chronic excess of calories over energy costs leads to additional accumulation of TG in adipose tissue - obesity. By