Review article: The role of adipose tissue in uraemia-related insulin resistance.
Adipose tissue is no longer considered to be an inert tissue of which function is to store fat. It actively secretes a number of biologic active compounds that are involved in the regulation of many processes like food intake, energy expenditure, metabolism homeostasis, immunity and blood pressure homeostasis. General metabolism alteration in patients with chronic kidney disease has a profound impact on biology of adipocytes. Chronic renal failure is a pathological condition, of which two major hallmarks are chronic inflammation and insulin resistance. In uraemic patients, adipose tissue became an important source of molecules that are responsible, at least in part, for the metabolic disturbances seen in these patients. Some of these molecules act as pro-inflammatory agents contributing to the maintenance and enhancement of the chronic inflammatory response. These pro-inflammatory molecules, along with other molecules secreted by the adipose tissue, have a central position in the aetiology of uraemia-associated insulin resistance. In this review, we intend to summarize some aspects of the biology of adipokines in uraemia, with emphasis on the link between these molecules and insulin resistance.
Manolescu
Bogdan
B
Department of Biochemistry, Faculty of Medicine, UMF Carol Davila, Bucharest, Romania. manolescub@yahoo.fr
Stoian
Irina
I
Atanasiu
Valeriu
V
Busu
Carmina
C
Lupescu
Olivera
O
D052242:Adiponectin / Q000502:physiology; D000273:Adipose Tissue / Q000502:physiology*; D006801:Humans; D007333:Insulin Resistance; D020738:Leptin / Q000502:physiology; D054409:Nicotinamide Phosphoribosyltransferase / Q000502:physiology; D052243:Resistin / Q000502:physiology; D014511:Uremia / Q000378:metabolism*
D052242:Adiponectin; D020738:Leptin; D052243:Resistin; D054409:Nicotinamide Phosphoribosyltransferase