Csaba Varga, PhD, Anikó Pósa, PhD, Krisztina Kedvesné Kupai: The metabolic syndrome
- The metabolic syndrome
- I. Introduction
- II. Historical survey
- III. Physiological basics
- III.1. Energy storage
- III.2. Regulation of lipid metabolism
- III.2.A. Adipose tissue distribution
- III.2.B. The endocrine function of adipose tissue
- III.2.B.a. Adiponectin
- III.2.B.b. Leptin
- III.2.B.c. Resistin
- III.2.B.d. Retinol binding protein 4 (RBP4)
- III.2.B.e. The complement system
- III.2.B.f. Interleukin-6 (IL-6)
- III.2.B.g. Monocyte chemoattractant protein-1 (MCP-1)
- III.2.B.h. Tumor necrosis factor-alpha (TNF-α)
- III.2.B.i. Plasminogen activator inhibitor type 1 (PAI-1)
- III.2.B.j. Angiotensinogen
- III.3. The glucose metabolism
- III.3.A. Transporters playing a role in Glu uptake and release
- III.3.B. Role of the pancreas
- III.3.C. Effects of catecholamines
- III.3.D. The renin-angiotensin-aldosterone system (RAAS)
- III.3.E. The effect of the growth hormone on the blood glucose level
- III.3.F. The effects of glucocorticoids
- III.3.G. The effects of thyroid hormones
- III.3.H. Regulation of the blood glucose level
- III.4. Hormonal regulation of the gastrointestinal system
- III.4.A. Gastrin
- III.4.B. Secretin
- III.4.C. Cholecystokinin (CCK)
- III.4.D. Gastric inhibitory peptide (GIP)
- III.4.E. Vasoactive intestinal peptide (VIP)
- III.4.F. Peptide histidine methionine
- III.4.G. Glucagon and enteroglucagon
- III.4.H. Pancreatic polypeptide (PP)
- III.4.I. Neuropeptide Y (NPY)
- III.4.J. Peptide tyrosine-tyrosine (PYY)
- III.4.K. Opioid peptides
- III.4.L. Motilin
- III.4.M. Metabolic effects of hormones
- III.5. The regulation of eating
- IV. Definition of the metabolic syndrome
- V. Parameters influencing the metabolic syndrome
- VI. Endothelial dysfunction in the metabolic syndrome
- VII. Cardiovascular risk factors
- VII.1. Hyperinsulinemia
- VII.2. ACE gene polymorphism
- VII.3. Microalbuminuria (MA)
- VII.4. Impaired glucose tolerance (IGT)
- VII.5. Type 2 diabetes mellitus (T2DM)
- VII. 6. Hyperlipidemia
- VII.7. Dyslipidemia
- VII.8. High cholesterol level
- VII.9. Nonalcoholic fatty liver disease (NAFLD)
- VII.10. Atherothrombosis and atherosclerosis
- VII.11. High blood pressure
- VII.12. Malnutrition
- VII.13. Lipoprotein a (Lpa)
- VII.14. Homocysteine (Hcy)
- VII.15. Hyperuricemia
- VII.16. Smoking
- VII.17. Stress
- VII.18. Depression
- VII.19. Age and sex
- VII.20. Lack of sleep
- VII.21. Obstructive sleep apnea (OSA)
- VII.22. Physical inactivity
- VIII. Cardiovascular complications
- IX. Inflammation and the metabolic syndrome
- X. The diagnostic parameters of the Metabolic syndrome
- XI. Prevention of the metabolic syndrome
- XII. Treatment of the metabolic syndrome
- XIII. Abbreviations
- XIV. References
- XV. Acknowledgments
VII.4. Impaired glucose tolerance (IGT)
IGT is a risk factor for CVD. A 6-7% increase in HBA1c is an important risk factor for infarct and stroke. The after-eating (postprandial) Glu level is more closely correlated with CVD than an impaired fasting Glu (IFG) level. If the fasting Glu level is in the normal range, but 2 h after the OGTT the blood Glu level is increased (7.5-11.1 mmol/l), the risk of CVD-caused death is enhanced twofold. A postprandial high blood Glu level increases the thickness of the carotis intima.
Készült az Új generációs sporttudományi képzés és tartalomfejlesztés, hazai és nemzetközi hálózatfejlesztés és társadalmasítás a Szegedi Tudományegyetemen c. pályázat támogatásával. Pályázati azonosító: TÁMOP-4.1.2.E-15/1/Konv-2015-0002