[Molecular biological approach to impaired glucose tolerance].
It is necessary to investigate the pathophysiology of impaired glucose tolerance (IGT) because the number of patients with IGT is larger than that of non-insulin-dependent diabetes mellitus (NIDDM) and the subjects with IGT are more likely to progress to overt NIDDM than those with normal glucose tolerance. IGT is a more heterogeneous state in volving various degrees of beta-cell dysfunction and insulin resistance, compared with NIDDM, therefore the approach to the candidate genes whose mutation increases the risk of developing IGT is with difficulty. We describe the direct screening of candidate genes with molecular biological method involved in insulin action, insulin secretion, obesity and adipocyte function, and the prospect of gene targeting study than can clarify the function of a single candidate gene.
Internal Medicine II, Kobe University School of Medicine.
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Mori
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Kasuga
D015415:Biomarkers; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics; D005941:Glucokinase / Q000235:genetics; D018149:Glucose Intolerance / Q000235:genetics*; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D009004:Monosaccharide Transport Proteins / Q000235:genetics; D011972:Receptor, Insulin / Q000235:genetics; D011943:Receptors, Adrenergic, beta / Q000235:genetics; D022702:Receptors, Adrenergic, beta-3
D015415:Biomarkers; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D011943:Receptors, Adrenergic, beta; D022702:Receptors, Adrenergic, beta-3; D005941:Glucokinase; D011972:Receptor, Insulin