Insulin Resistance Syndrome

Posted by e-Medical PPT
ACE position statement
Clinical manifestations include CVD, hypertension, PCOS, and nonalcoholic steatohepatitis NASH, and the list continues to expand.
(AACE) championed the creation of the new ICD-9 Code 277.7 for the “Dysmetabolic Syndrome”
use the term Insulin Resistance Syndrome to describe the consequences of insulin resistance and compensatory hyperinsulinemia
absence of a straightforward diagnostic test or definitive clinical trials, identification and treatment of a syndrome

Obesity and Insulin Resistance Syndrome
Obesity is a physiological variable that decreases insulin-mediated glucose disposal
BMI rather than abdominal circumference, be used to identify individuals at increased risk
Abdominal circumference are neither routinely performed nor is its quantification as well standardized
European Group for the Study of IR was not increased when abdominal circumference replaced BMI as the marker of obesity
BMI and abdominal circumference were closely related r=0.9 in 15,271 participants in NHANES III

Plasma insulin concentration and the IRS
Plasma insulin concentrations are useful surrogate marker of IR
Highly statistically significant correlations between measures of insulin-mediated glucose disposal and both fasting (r=0.6) and post-glucose challenge (r=0.8) plasma insulin concentrations
Methods to quantify plasma insulin concentrations are not standardized
Difficult to compare values measured in different clinical laboratories
Has not been established that an increase in plasma insulin concentration, by itself, in the absence of any of changes listed in Table 3, can predict the development of CVD
A research, not a clinical tool

Factors that increase the likelihood of IRS
include having CVD
Hypertension
polycystic ovarian syndrome
acanthosis nigricans
a family history of type 2 diabetes, hypertension, or CVD
a history of gestational diabetes or glucose intolerance
non-Caucasian ethnicity
sedentary lifestyle
obesity

Table of content
Determinants of insulin sensitivity
Mechanisms of insulin resistance
Endothelial dysfunction and insulin resistance
Nonalcoholic fatty liver disease
Lifestyle approaches for the IRS
Low-carbohydrate diet for atherogenic dyslipidemia
Relationship between obesity and the IRS
Adipocyte hormones and insulin action
Inflammation and the IRS

Mechanisms of insulin resistance
Carbon NMR studies with a profound defect in muscle glycogen synthesis in persons with type 2 diabetes
Phosphorus NMR studies suggest transport defects at the level of hexokinase or GLUT4 to be primary 
offspring of persons with type 2 diabetes suggest this abnormality to precede the onset of the disease
Further 13C NMR spectroscopy has suggested that the defect is at the level of GLUT4.
The abnormality in GLUT4 is strongly predicted by the free fatty acid (FFA) level and, even more strongly, by intramyocellular triglyceride levels
A potential mechanism by which fatty acid metabolites inhibit glucose transport activity appears to involve the insulin signaling cascade, with decreased phosphatidylinositol 3-kinase caused by activation of a serine kinase cascade via protein kinase C-[theta] decreasing the translocation of GLUT4 to the cell membrane.
peroxisome proliferator-activated receptor [gamma] agonists act by increasing adipose tissue fat stores and preventing the increase in fatty acid metabolites in liver and muscle.

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