2004
DOI: 10.1590/s0100-879x2004000500006
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Comparison of the homeostasis model assessment and quantitative insulin sensitivity check index with data from forearm metabolic studies for the in vivo assessment of insulin sensitivity

Abstract: The present study was designed to compare the homeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI) with data from forearm metabolic studies of healthy individuals and of subjects in various pathological states. Fifty-five healthy individuals and 112 patients in various pathological states, including type 2 diabetes mellitus, essential hypertension and others, were studied after an overnight fast and for 3 h after ingestion of 75 g of glucose, by HOMA, QUICKI and the for… Show more

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Cited by 7 publications
(6 citation statements)
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References 32 publications
(26 reference statements)
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“…The HOMA estimate of insulin sensitivity significantly correlates with data derived from forearm metabolic studies involving direct measurements of insulin action on muscle glucose metabolism (35). The finding of higher insulin sensitivity after 1 week of HSD than after 13 weeks, with no changes in body weight, appears to indicate that the positive effect of salt on insulin sensitivity is transitory, at least in the elderly volunteers studied.…”
Section: Discussionsupporting
confidence: 52%
“…The HOMA estimate of insulin sensitivity significantly correlates with data derived from forearm metabolic studies involving direct measurements of insulin action on muscle glucose metabolism (35). The finding of higher insulin sensitivity after 1 week of HSD than after 13 weeks, with no changes in body weight, appears to indicate that the positive effect of salt on insulin sensitivity is transitory, at least in the elderly volunteers studied.…”
Section: Discussionsupporting
confidence: 52%
“…We collected sequential sagittal sections every 20 μm for H&E staining. HOMA-IR was calculated as described 58 . Serum and tissue lipids, ALT and AST were measured using commercial kits as described previously 59 .…”
Section: Methodsmentioning
confidence: 99%
“…Both in vitro and in vivo studies show that exposure to hyperglycemia reduces endothelial NO availability and its bioactivity (Williams et al, 1998, Veves et al, 1998. The control of blood glucose homeostasis is mainly determined by two closely related physiological mechanisms: the capacity of the pancreas to secrete insulin and the biological action of this hormone on insulin-sensitive tissues, especially liver, muscle and adipose tissue (Foss-Freitas, 2004). It is well known that in type 2 diabetes mellitus and in metabolic syndrome, as well as in various other human pathological states such as glucose intolerance, obesity, polycystic ovary syndrome, essential hypertension, and, more recently, atherosclerosis, insulin resistance is either an associated condition or is considered to be a predictor or pathogenic factor (De Fronzo, 1988, 1991, Guizea, 2008.…”
Section: Introductionmentioning
confidence: 99%
“…Insulin resistance in muscle cells reduces the glucose uptake, whereas in liver cells results in impaired glycogen synthesis and a failure to suppress glucose production. All these phenomena lead to reduced muscle glucose uptake and increased liver glucose production, thus contributing to the elevation of the blood glucose level, and accelerating the glucose toxicity associated with the insulin resistance (Freitas 2004, De Fronzo 1988, 1991, Guizea 2008. The medical community agrees that the evaluation of the insulin resistance phenomena might be important for the assessment of hyperglycemia patients.…”
Section: Introductionmentioning
confidence: 99%
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