Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin clamp studies were carried out on 13 non-diabetics and 12 non-insulin-dependent diabetics (NIDDM). Based upon the body mass index (BMI), they were further divided into obese (BMI greater than or equal to 27 kg/m2) and nonbese groups (BMI less than 27 kg/m2). All received euglycemic insulin clamp study (Humulin-S 40mU/m2/min). Thermoregulated venous samplings were done every five minutes for measurements of plasma glucose (PG) and immunoreactive insulin (IRI). Steady state plasma glucose (SSPG) was obtained 20-80 minutes and kept for 100 more minutes. The data of final 40 minutes of clamp were used for analysis. Variations in SSPG and metabolic clearance rate of glucose (MCRG) instead of glucose infusion rate (M) value were used to assess the insulin sensitivity. The results showed that insulin resistance was noted in obese non-diabetic and diabetic subjects as well as in non-obese diabetic patients, as evidenced by higher basal IRI and lower MCRG than non-obese normal controls. Correlation analysis revealed that there was no correlation between the reduction of MCRG and the BMI in either non-diabetic or diabetic patients. There was a strong negative correlation between MCRG and the ambient fasting plasma glucose in the diabetic group, whereas this correlation was not found in the non-diabetic group. In conclusion, obesity with or without diabetes did have remarkable insulin resistance. In non-diabetic obese subjects the insulin resistance did not go up as the BMI increased further. In diabetic patients, both obesity and hyperglycemia contributed significantly insulin resistance.
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PMID:Insulin resistance in obesity and noninsulin dependent diabetes mellitus. 276 59

The prevalence of obesity and diabetes has been dramatically increasing during the last decade suggesting a greater patient need for more efficacious and safer drugs. Large molecule therapy has played an important role in diabetes since the discovery of insulin. This legacy was continued upon the introduction of Humulin (first recombinant insulin), Humalog (first engineered insulin) and Byetta (first incretin mimetic). Several other protein therapeutics, such as leptin, adiponectin, bone morphogenic protein-9 and others, are currently in or considered for therapeutic development. Among them, FGF21 is one of the most promising candidates given its outstanding pharmacologic benefits for nearly each and every abnormality of a metabolic disease and lack of apparent side effects in a variety of animal models. Thus, FGF21 represents a novel and appealing therapeutic reagent for Type 2 diabetes mellitus, obesity, dyslipidemia, cardiovascular and fatty liver diseases. The in vitro biology, genetic animal models and in vivo pharmacology of FGF21 will be discussed in this chapter.
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PMID:FGF21 as a therapeutic reagent. 2239 72