glitazones

glitazones

Thiazolidinedione derivative drugs used to treat type II (non-insulin-dependent) diabetes mellitus. Glitazones act by altering fatty acid metabolism by way of peroxisome proliferator-activated receptors which, in effect, increase cell sensitivity to insulin.
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Exclusion criteria for the subjects were subjects undergoing regular exercise, subjects on medications such as statins, glitazones, fibrates, niacin, clopidogrel, aspirin, iron/vitamins supplements, and antihypertensives, and subjects having a history of any major disease such as ischemic heart disease, hypertension, kidney or liver disease, diabetes mellitus, dyslipidemia, malignancy, venous thrombosis, systemic or pulmonary embolism, congenital hemorrhagic disease, and thrombocytopenia.
Glitazones are different: they improve insulin sensitivity and can promote the conversion of unhealthy white adipose tissue into fat-burning beige adipocytes.
This signifies that osteoporosis also depend on some other factors like increasing age, female gender, menopause, low BMI, low calcium diet, lack of exercise, decreased sunlight exposure, medications like steroid, glitazones etc.
As already said, the risk was much higher in case of sulphonylurea, either alone or in association with metformin, while it remained rather low and almost stable over time in patients on diet or glitazones or metformin alone.
However, it has been also reported that, despite use of high doses of insulin or oral drugs like metformin and glitazones, poor glycemic control persisted in most patients with RMS (2).
(10,35 Notably, the antidiabetic glitazones, especially rosiglitazone, can boost LDL-C or triglycerides.
Thiazolidinediones (glitazones), such as rosiglitazone and pioglitazone, have been widely used as insulin sensitizers and activators of PPAR[gamma].
Range of drugs like sulfonylureas, biguanides, glinides, and glitazones are used for the treatment of type 2 diabetes but all of them suffer from unintended effects like hypoglycemia and obesity [3-6].
This is a potential interaction point especially in diabetes patients on OADs because glitazones like rosiglitazone are largely metabolized by CYP2C8 and to a lesser extent by CYP2C9 [209].
This is the case of the PPAR[gamma] activators known as glitazones, for which the inhibition of the mitochondrial MAO belongs to the list of their "off-target" actions [54], together with their neuroprotective secondary effects [55].