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The deposition (storage) of fats.



There are two mechanisms of fat storage; capture them (triacylglycerides) from the plasma and lipogenesis - the synthesis of fats from other sources, in particular, glucose.
Fatty tissue is a kind of self-loading energy battery, it constantly participates in the metabolism. In the resting condition, after eating, 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 largest amount of triacylglycerides) are too large to penetrate from the capillaries into the intercellular fluid, and from there to the fat cells (adipocytes).
But there is a mechanism to overcome this difficulty. Fat cells (adipocytes) secrete one enzyme, a lipoprotein lipase, that splits lipoprotein particles to free fatty acids, and they can freely penetrate into the intercellular fluid and reach adipocytes.

Getting into fat cells, (adipocytes) fatty acids are collected in lipid droplets to accumulate in the cell.
The activity of lipoprotein lipase in adipose tissue is regulated than you think ?! Insulin, released in response to an increase in blood glucose. Since we rarely eat pure fat, after regular meals containing both fats and carbohydrates, the capture of fats in adipose tissue is stimulated by insulin. The effect of insulin on the activity of the enzyme (lipoprotein lipase) is to enhance the isolation 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, fatty acid esterification is also stimulated in insulin by insulin
Confused?
The main thing that follows from this is to understand that insulin stimulates and captures, and accumulates fats circulating in the blood in adipose tissue.
Another possible mechanism of fat deposition - lipogenesis or pentose phosphate pathway, is also stimulated by insulin.
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The deposition (storage) of fats.

  1. Fat 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 combining infiltration with a violation of the structure of the protoplasm and its protein component, one speaks of fatty degeneration. The common cause of fatty infiltration and fatty dystrophy is the suppression of the activity of oxidative and hydrolytic enzymes of lipid metabolism
  2. Arthropathy with deposition of crystals
    Intraarticular deposits of crystals are associated with a number of acute and chronic changes in the joints. Endogenous crystals causing pathological changes are crystals of monosodium urates (uric acid salts), calcium pyrophosphate dehydrate and basic calcium phosphate (hydroxyapatite). Exogenous crystals of esters of corticosteroids, talc, polyethylene and methyl methacrylate can also
  3. Fat embolism (traumatic). Other obstetric embolism. Obstetric fat embolism
    ICD-10 cipher Fat embolism (traumatic) T79.1 Other obstetric embolism. Obstetric fatty embolus O88.8 Diagnosis When establishing a diagnosis Obligatory history (trauma, childbirth, osteometallosynthesis, extensive burns, severe metabolic disorders, IV injection of fat emulsions, closed cardiac massage, etc.), blood pressure, heart rate, BH, examination of the skin and mucous membranes (eruptions)
  4. Subcutaneous fat layer:
    • the degree of development, the nature of the spread, the thickness of the subcutaneous fat fold on the abdomen, on the chest, back, limbs, face; • the presence of edema and seals; • Turgor of tissues. Some idea of ​​the amount and distribution of the subcutaneous fat layer can be obtained by general examination of the child, but the final judgment on the state of the subcutaneous fat layer is done only after palpation. For
  5. Fat embolism
    The syndrome of fat embolism can develop from 1 hour to 3 days after injury. Although fat embolism is more often associated with fracture of tubular bones or pelvis, it has also been reported on its causes, such as diabetes, fatty liver, pancreatitis, joint surgery, sickle cell anemia. It is theorized that lung damage develops when lipases hydrolyse neutral
  6. Absorption of fats
    Fats in food consist mainly of triglycerides, phospholipids (lecithin) and cholesterol (as esters) (Figure 6-17). For a complete digestion and absorption of fats, a combination of several factors is necessary: ​​normal liver and biliary tract functioning, the presence of pancreatic enzymes and alkaline pH, the normal state of enterocytes, the lymphatic system of the intestine and the functional
  7. FATTY EMBOLY SYNDROME
    The syndrome of fat embolism (SZE) is a clinically manifested systemic intravascular dissemination of globules of neutral fat inside microvessels. Fat embolism is a recognition of the fact of embolization, but without clinical manifestations. Etiopathogenesis. Most often, SCF develops with fractures of long tubular bones of the lower extremities, pelvic bones. The risk of developing the syndrome increases with
  8. Fat embolism
    Symptoms of fat embolism: • ???? arterial hypoxemia (this sign may be the only one); • acute acute respiratory distress syndrome; • ???? violation of the central nervous system (motor anxiety, coma, epiprip); • ???? petechiae (neck, forearm, thorax); • coagulopathy;
  9. Liver dystrophy (steatosis)
    Causes: Unsustainable use of alcohol, fatty foods, overweight, diabetes mellitus, prolonged exposure to chemicals, solvents such as benzene, tetrachloride, chloroform, effects of cortisone (or tetracycline) medication. As a rule, after eliminating the cause, fat deposits in the liver disappear. In severe form, malaise develops in cirrhosis of the liver. Further there is
  10. Violations of the accumulation of fat in fatty tissue. OBESITY
    These disorders are manifested either in the form of exhaustion as an extreme variant of losing weight, or in the form of obesity. Depletion (see "Violations of protein metabolism") is observed when the intake of calories from food is insufficient in relation to energy needs. Chronic excess of the intake of calories over energy costs leads to an additional accumulation of TG in adipose tissue - obesity. By
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