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Research Article Open access CC BY 4.0

Role of Hypoxia Inducible Factors in Obesity Pathogenesis

Hande O. Altunkaynak, Nuray Yazihan

Journal of Advances in Medicine and Medical Research · pp. 1–8 · Published 28 Apr 2016

10.9734/BJMMR/2016/25427

Abstract

The prevalence of obesity, metabolic syndrome and diabetes has been increasing rapidly worldwide. These are a group of metabolic disorders characterized by a chronic hyperglycaemic condition resulting from defects in insulin secretion, insulin action or both. The control of body weight and blood glucose concentrations depends on the exquisite coordination of the function of several cells, organs and tissues. Underlying mechanisms of obesity and insulin resistance remain uncertain. Adipose tissue is composed of heterogeneous cell types. Immune cells within adipose tissue also likely contribute to systemic metabolic processes. Increased production of local and systemic adipokines and cytokines, polarization of macrophages, T helper subtype changes could contribute to pathologies linking obesity to diabetes, both by decreasing insulin sensitivity, by compromising β-cell function and disturbing adipose tissue metabolism and distribution. Tissue oxygen (O2) levels, hypoxia inducible factor (s) (HIFs) secretion differences regulate the plasticity of macrophages and the polarization of macrophages controls functionally divergent processes in cells. A hypoxic and inflammatory phenotype has been reported in adipose tissue during obesity. Therefore, the present review focuses HIFs-mediated effects of hypoxia in adipocyte inflammation and macrophage polarization associated with obesity pathogenesis.

Obesity pathogenesis hypoxia inducible factors inflammation

References (54)

  1. 1 Inflammation and metabolic disorders [DOI]
  2. 2 Obesity is associated with macrophage accumulation in adipose tissue [DOI]
  3. 3 Adipose Expression of Tumor Necrosis Factor-α: Direct Role in Obesity-Linked Insulin Resistance [DOI]
  4. 4 Targeting of HIF-α to the von Hippel-Lindau Ubiquitylation Complex by O 2 -Regulated Prolyl Hydroxylation [DOI]
  5. 5 The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis [DOI]
  6. 6 Paradoxical Decrease of an Adipose-Specific Protein, Adiponectin, in Obesity [DOI]
  7. 7 Inflammation, stress, and diabetes [DOI]
  8. 8 Critical nodes in signalling pathways: insights into insulin action [DOI]
  9. 9 Macrophages, Inflammation, and Insulin Resistance [DOI]
  10. 10 Adipokines: inflammation and the pleiotropic role of white adipose tissue [DOI]
  11. 11 Adipose tissue remodeling and obesity [DOI]
  12. 12 Differential Function of the Prolyl Hydroxylases PHD1, PHD2, and PHD3 in the Regulation of Hypoxia-inducible Factor [DOI]
  13. 13 Hypoxia Inducible Factor-α Binding and Ubiquitylation by the von Hippel-Lindau Tumor Suppressor Protein [DOI]
  14. 14 Inflammation and Lipid Signaling in the Etiology of Insulin Resistance [DOI]
  15. 15 Apelin, a Newly Identified Adipokine Up-Regulated by Insulin and Obesity [DOI]
  16. 16 Hypoxia and Adipose Tissue Function and Dysfunction in Obesity [DOI]
  17. 17 HIF-2α Promotes Hypoxic Cell Proliferation by Enhancing c-Myc Transcriptional Activity [DOI]
  18. 18 Toll-like receptor–induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens [DOI]
  19. 19 Alternative Macrophage Activation and Metabolism [DOI]
  20. 20 Increased Adipocyte O2 Consumption Triggers HIF-1α, Causing Inflammation and Insulin Resistance in Obesity [DOI]
  21. 21 Orchestration of Metabolism by Macrophages [DOI]
  22. 22 ARGINASE: A CRITICAL REGULATOR OF NITRIC OXIDE SYNTHESIS AND VASCULAR FUNCTION [DOI]
  23. 23 Obesity Decreases Perioperative Tissue Oxygenation [DOI]
  24. 24 Regulation of Resistin Expression and Circulating Levels in Obesity, Diabetes, and Fasting [DOI]
  25. 25 Glucose Uptake and Perfusion in Subcutaneous and Visceral Adipose Tissue during Insulin Stimulation in Nonobese and Obese Humans [DOI]
  26. 26 Complementary roles of IRS-1 and IRS-2 in the hepatic regulation of metabolism [DOI]
  27. 27 Hypoxia-inducible Factor 1 Transactivates the Human Leptin Gene Promoter [DOI]
  28. 28 S-Nitrosylation-dependent Inactivation of Akt/Protein Kinase B in Insulin Resistance [DOI]
  29. 29 Adipose tissue hypoxia induces inflammatory M1 polarity of macrophages in an HIF-1α-dependent and HIF-1α-independent manner in obese mice [DOI]
  30. 30 Regulation of HIF-1α activity in adipose tissue by obesity-associated factors: adipogenesis, insulin, and hypoxia [DOI]
  31. 31 Roles of the human hypoxia-inducible factor (HIF)-3α variants in the hypoxia response [DOI]
  32. 32 Transcriptional Activation of the Human Leptin Gene in Response to Hypoxia [DOI]
  33. 33 HIF-1 versus HIF-2 — Is one more important than the other? [DOI]
  34. 34 Cross-talk between hypoxia and insulin signaling through Phd3 regulates hepatic glucose and lipid metabolism and ameliorates diabetes [DOI]
  35. 35 Oxygen sensing and metabolic homeostasis [DOI]
  36. 36 Hearts of Hypoxia-inducible Factor Prolyl 4-Hydroxylase-2 Hypomorphic Mice Show Protection against Acute Ischemia-Reperfusion Injury [DOI]
  37. 37 Macrophage HIF-2α Ameliorates Adipose Tissue Inflammation and Insulin Resistance in Obesity [DOI]
  38. 38 Targeted Disruption of the Tumor Necrosis Factor-α Gene: Metabolic Consequences in Obese and Nonobese Mice [DOI]
  39. 39 Hypoxia, HIF-1, and the Pathophysiologi of Common Human Diseases [DOI]
  40. 40 Hypoxia inducible factor-2α: a critical mediator of aggressive tumor phenotypes [DOI]
  41. 41 Hypoxia increases leptin expression in human PAZ6 adipose cells [DOI]
  42. 42 Deletion of Hypoxia-Inducible Factor-1α in Adipocytes Enhances Glucagon-Like Peptide-1 Secretion and Reduces Adipose Tissue Inflammation [DOI]
  43. 43 Loss of von Hippel-Lindau Protein (VHL) Increases Systemic Cholesterol Levels through Targeting Hypoxia-Inducible Factor 2α and Regulation of Bile Acid Homeostasis [DOI]
  44. 44 Signalling Cross Talk of the HIF System: Involvement of the FIH Protein [DOI]
  45. 45 Hypoxia-inducible Factor-2α-dependent Hypoxic Induction of Wnt10b Expression in Adipogenic Cells [DOI]
  46. 46 Prolonged fasting activates hypoxia inducible factors-1α, -2α and -3α in a tissue-specific manner in northern elephant seal pups [DOI]
  47. 47 Ischemia‐Reperfusion Injury of Adipofascial Tissue: An Experimental Study Evaluating Early Histologic and Biochemical Alterations in Rats [DOI]
  48. 48 HIF-2α Blows Out the Flames of Adipose Tissue Macrophages to Keep Obesity in a Safe Zone [DOI]
  49. 49 HIF-2α regulates Oct-4: effects of hypoxia on stem cell function, embryonic development, and tumor growth [DOI]
  50. 50 Differential activation and antagonistic function of HIF-α isoforms in macrophages are essential for NO homeostasis [DOI]
  51. 51 Insulin resistance and atherosclerosis [DOI]
  52. 52 HIF Prolyl 4-Hydroxylase-2 Inhibition Improves Glucose and Lipid Metabolism and Protects Against Obesity and Metabolic Dysfunction [DOI]
  53. 53 β-adrenergic stimulation and abdominal subcutaneous fat blood flow in lean, obese, and reduced-obese subjects [DOI]
  54. 54 Hypoxia-Inducible Factor-3.ALPHA. Functions as an Accelerator of 3T3-L1 Adipose Differentiation [DOI]

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