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🏥 | Two exercise methods to "reduce visceral fat" Recommended by cardiologists


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Two exercises to "reduce visceral fat" Recommended by cardiologists

 
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What is the relationship between increasing hormone-like substances secreted by fat cells and exercise habits?
 

[Maintenance of the body to keep illness away] Blood vessels (upper) The coronary arteries that send blood and oxygen to the heart muscle (heart muscle) are clogged ... → Continue reading

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We will deliver the medical and health articles of the evening paper "Daily Gendai". From everyday health laws to the latest medical information, all articles are based on interviews with doctors and specialists.


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Fat cells

Fat cells(Shibosaibo,British: adipocyte) IsCytoplasmHave in細胞That is.

Monocystic adipocytes (white adipocytes) and polyvesicular adipocytes (Brown fat cells) And.Monocystic adipocytes have large lipid dropletsNuclear,OrganelleIs a storage-type cell whose margin is compressed, and a multivesicular adipocyte is a metabolic-type cell in which a large number of small or medium-sized lipid droplets are present and organelles are developed.

hibernationMainly polyvesicular adipocytes in animalsAdipose tissueIs sometimes called the hibernating gland.In recent years, many adipose stem cells have been found in adipose tissue,Adipose stem cell transplantAs a cell source (cell source) for regenerative medicine, its value has attracted attention.[1].

Hypertrophy of fat cells

Preadipocytes promote fatty acid transport to adipocytesTranscription factorIsPPARγIt becomes mature adipocytes (normal adipocytes) by being stimulated by factors such as.Chylomicron,VLDL OfNeutral fatIs degraded by lipoprotein lipasefatty acidTo the adipocytes, the adipocytes mature.Also,glucoseIs taken up by adipocytes to synthesize fatty acids.Normal fat cellsInsulin receptorPromotes glucose uptake without the intervention of, and also improves the sensitivity of insulin receptorsAdiponectinSecrete.Fat cells gradually become hypertrophied due to high calorie intake and lack of exercise, and become hypertrophied fat cells.When the size of adipocytes reaches the upper limit and no more fat can be stored, the surrounding preadipocytes are stimulated by PPARγ or the like to become mature adipocytes and gradually enlarge.Also, fat cellsCell divisionHowever, the number of fat cells also increases.

There are 250-300 billion white adipocytes in humans, 70-90 μm in diameter in mature adipocytes, and hypertrophied adipocytes up to 130-140 μm.The diameter of brown adipocytes is 20-40 μm[2].

Hypertrophic adipocyte secretion

When fat cells become hypertrophied,Insulin resistanceVarious substances that causeTNFα,fatty acid,), Stimulates the obesity center and suppresses appetiteLeptin, Improves insulin receptor sensitivityAdiponectinSubstances that promote decreased secretion and blood coagulation (en: plasminogen activator A substance that inhibits the dissolution of blood coagulation),Monocyte,lymphocytesMonocyte chemoattractant protein, a bioactive substance with pressor actionAngiotensinAngiotensinogen, which is the raw material of II, is secreted[2].

Relationship with high blood pressure

When fat cells become hypertrophied, the following things happen in relation to blood pressure:

AngiotensinogenliverIt is also produced and secreted from hypertrophied adipocytes.Produced from angiotensinogenAngiotensinⅡ isAdrenal cortexActs on the zona glomerulosa to promote sodium reabsorptionAldosteronePromotes the secretion of water and stores water in the body[4]. Also,Pituitary glandIt is an antidiuretic hormone that acts on and suppresses diuresis.VasopressinPromotes the secretion of (ADH) and also stores water in the body[5].

By these thingsHigh blood pressureInvite.obesityThis is why patients often have hypertension.[2].

Also, due to the enlargement of mast cells (= obesity)Insulin resistanceThe expression ofHyperinsulinemiaTo bring up.Hyperinsulinemia is the kidneyRenal tubuleActs directly onsodiumCauses retention, which stores water as a resultBlood glucose levelHowever, the accumulation of water causes hypertension.[6].

Relationship with insulin resistance

When fat cells become hypertrophied, free fatty acids are released, especially from the fat cells present in the internal organs.Part of this fatty acid is transported to skeletal muscle and hepatocytes, and the fatty acid transported into skeletal muscle is an enzyme that phosphorylates protein molecules.Protein kinaseActivate C and furtherNF-κBIκBα related toSerineAn enzyme complex that phosphorylates residuesIκB kinase (IKK) is activated and is an insulin receptor substrateIRS1Phosphorylates serine residues in proteins.Phosphorylation of the IRS1 protein by this pathway interferes with the normal phosphorylation process, resulting in the loss of IRS1 and subsequent signals and insulin dependence.Glucose transporterIsGLUT4Cannot be transferred to the membrane. When GLUT4 becomes difficult to function, insulin causesglucoseIs less likely to be taken up by cells.This state isInsulin resistanceBecome[2].

As another mechanism, MCP-1, a monocyte chemotactic protein, is released from adipocytes, and MCP-1 is released.MonocyteThe monocytes that have been attracted to the outside of the cell are activated.MacrophageWill be.These macrophages accumulate around fat cells and from hereTumor necrosis factorKnown asTNFαSecrete. When TNFα binds to the receptor, JNK (c-Jun amino-terminal kinase), which is a serine-threonine kinase, phosphorylates the serine residue of the IRS1 protein, which is an insulin receptor substrate.This pathway also results in insulin resistance, similar to the mechanism described above.TNFα also has the effect of suppressing the expression of GLUT4. These effects of TNFα show marked insulin resistance[2].

In addition, it is secreted by fat cellsAdiponectinUnlike TNFα and free fatty acids, it increases the sensitivity of insulin receptors, but the hypertrophy of adipocytes reduces the secretion of adiponectin, resulting in insulin resistance.[2].

footnote

  1. ^ Edited by the Japanese Society of Veterinary Anatomy "Veterinary Histology Revised Second Edition" Gakudosha 2003 ISBN 4873621135
  2. ^ a b c d e f Adipocytes and insulin resistanceKoshio Kamata, Open Research Center, Star University of Pharmacy
  3. ^ Yoshihiro Ogawa, "Leptin and cardiovascular lesions"Journal of the Japanese Society of Internal Medicine" 2001 Volume 90 Issue 4 p.705-710, two:10.2169 / naika.90.705, Japanese Society of Internal Medicine
  4. ^ Research topics Elucidation of the mechanism of blood pressure increase due to excessive salt intakeToshiro Fujita, Department of Nephrology and Endocrinology, The University of Tokyo Hospital Graduate School of Medicine / Faculty of Medicine Hospital
  5. ^ Discover a new action in the brain of the hormone vasopressin that suppresses diuresisNational Institute for Physiological Sciences, National Institute of Natural Sciences Yasunobu Okada et al.
  6. ^ Basic knowledge of diabetesKoshio Kamata, Open Research Center, Star University of Pharmacy[Broken link]

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