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- W1998221258 abstract "Type II (non-insulin-dependent) diabetes mellitus is associated with increased blood concentrations of markers of the acute-phase response, including sialic acid, α-1 acid glycoprotein, serum amyloid A, C-reactive protein and cortisol, and the main cytokine mediator of the response, interleukin-6. The dyslipidaemia common in Type II diabetes (hypertriglyceridaemia and low serum levels of HDL cholesterol) is also a feature of natural and experimental acute-phase reactions. We review evidence that a long-term cytokine-mediated acute-phase reaction occurs in Type II diabetes and is part of a wide-ranging innate immune response. Through the action of cytokines on the brain, liver, endothelium, adipose tissue and elsewhere, this process could be a major contributor to the biochemical and clinical features of metabolic syndrome X (glucose intolerance, dyslipidaemia, insulin resistance, hypertension, central obesity, accelerated atherosclerosis) but also provides a mechanism for many other abnormalities seen in Type II diabetes, including those in blood clotting, the reproductive system, metal ion metabolism, psychological behaviour and capillary permeability. In the short-term, the innate immune system restores homeostasis after environmental threats; we suggest that in Type II diabetes and impaired glucose tolerance long-term lifestyle and environmental stimulants, probably in those with an innately hypersensitive acute-phase response, produce disease instead of repair. [Diabetologia (1998) 41: 1241–1248]" @default.
- W1998221258 created "2016-06-24" @default.
- W1998221258 creator A5024814684 @default.
- W1998221258 creator A5051150407 @default.
- W1998221258 date "1998-09-18" @default.
- W1998221258 modified "2023-10-14" @default.
- W1998221258 title "Is Type II diabetes mellitus a disease of the innate immune system?" @default.
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- W1998221258 doi "https://doi.org/10.1007/s001250051058" @default.
- W1998221258 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9794114" @default.
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