The role of complement factor C3 in lipid metabolism.
Abundant reports have shown that there is a strong relationship between C3 and C3a-desArg levels, adipose tissue, and risk factors for cardiovascular disease, metabolic syndrome and diabetes. The data indicate that complement components, particularly C3, are involved in lipid metabolism. The C3 fragment, C3a-desArg, functions as a hormone that has insulin-like effects and facilitates triglyceride metabolism. Adipose tissue produces and regulates the levels of complement components, which promotes generation of inflammatory initiators such as the anaphylatoxins C3a and C5a. The anaphylatoxins trigger a cyto/chemokine response in proportion to the amount of adipose tissue present, and induce inflammation and mediate metabolic effects such as insulin resistance. These observations support the concept that complement is an important participant in lipid metabolism and in obesity, contributing to the metabolic syndrome and to the low-grade inflammation associated with obesity.
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden. Electronic address: andreea.barbu@igp.uu.se.
Andreea
A
Barbu
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Osama A
OA
Hamad
Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
Lars
L
Lind
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Kristina N
KN
Ekdahl
Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Bo
B
Nilsson
D000273:Adipose Tissue / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D001053:Apolipoproteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D015926:Complement C3a / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015936:Complement C5a / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D003920:Diabetes Mellitus / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation; D006801:Humans; D007333:Insulin Resistance / Q000276:immunology; D050356:Lipid Metabolism / Q000276:immunology*; D024821:Metabolic Syndrome / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D011951:Receptors, Complement / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D012307:Risk Factors; D014280:Triglycerides / Q000235:genetics / Q000276:immunology / Q000378:metabolism
D001053:Apolipoproteins; D011951:Receptors, Complement; D014280:Triglycerides; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a; D015936:Complement C5a
Apolipoproteins; C3; C3a-desArg; Metabolic syndrome (MetS); Obesity