Patterns of Glucose and Lipid Abnormalities in Black NIDDM Subjects

Objective We had previously shown two variants among black non-insulin-dependent diabetic (NIDDM) subjects in a normoglycemic remission: one with insulin resistance and the other with normal insulin sensitivity. This study examined whether these two variants exist in the ordinary hyperglycemic black NIDDM population. Research Design and Methods Fifty-two black NIDDM subjects were assessed for insulin-stimulated glucose disposal (euglycemic clamp), glycemic control (fasting plasma glucose and HbA1c), and fasting lipid profiles. Results The distribution of glucose disposal in 30 black NIDDM subjects (body mass index; BMI < 30 kg/m2) was bimodal, which indicated two populations. Eighteen of 30 subjects (BMI 26.4 ± 0.5 kg/m2) had insulin resistance (glucose disposal 3.21 ± 0.24 mg·kg−1·min−1). Twelve of 30 subjects (BMI 24.83 ± 1.1 kg/m2) had normal insulin sensitivity (glucose disposal 7.19 ± 0.46 mg·kg−1·min−1). Twenty-one of the remaining 22 subjects (BMI 33.4 ± 0.7 kg/m2) were insulin resistant (glucose disposal 2.88 ± 0.21 mg·kg−1·min−1). Fasting serum triglyceride levels were lowest in the insulin-sensitive population (0.91 ± 0.07 mM) and different from the insulin-resistant population, BMI < 30 and > 30 kg/m2, (1.20 ± 0.10 mM, P < 0.05 and 1.42 ± 0.17 mM, P < 0.025, respectively). Fasting serum low-density lipoprotein cholesterol levels were not significantly different among the groups, although it did increase with insulin resistance and increasing obesity. Total serum cholesterol levels and glycemic control were similar for all three groups. Serum high-density lipoprotein cholesterol levels were higher in women compared with men. Conclusions In the hyperglycemic black NIDDM population, two variants exist: one with insulin resistance and one with normal insulin sensitivity. This insulin-sensitive variant represents 40% of subjects with a BMI < 30 kg/m2. Moreover, the insulin-sensitive group has a lower risk profile for cardiovascular disease.

[1]  Insulin-Sensitive and Insulin-Resistant Variants in NIDDM , 1989, Diabetes.

[2]  R. DeFronzo.  The Triumvirate: β-Cell, Muscle, Liver: A Collusion Responsible for NIDDM , 1988, Diabetes.

[3]  L. Mandarino,et al.  Quantification of the relative impairment in actions of insulin on hepatic glucose production and peripheral glucose uptake in non-insulin-dependent diabetes mellitus. , 1988, Metabolism: clinical and experimental.

[4]  R. Rizza,et al.  Insulin action in non-insulin-dependent diabetes mellitus: the relationship between hepatic and extrahepatic insulin resistance and obesity. , 1987, Metabolism: clinical and experimental.

[5]  S. Efendić,et al.  Glyburide Decreases Insulin Requirement, Increases (β-Cell Response to Mixed Meal, and Does Not Affect Insulin Sensitivity: Effects of Short- and Long-Term Combined Treatment in Secondary Failure to Sulfonylurea , 1987, Diabetes Care.

[6]  N. Maclaren,et al.  Maturity-onset diabetes of youth in black Americans. , 1987, The New England journal of medicine.

[7]  L. Groop,et al.  Effect of Glyburide on Glycemic Control, Insulin Requirement, and Glucose Metabolism in Insulin-Treated Diabetic Patients , 1987, Diabetes.

[8]  G. Reaven,et al.  A Comparison of the Relative Effects of Obesity and Non-insulin-dependent Diabetes Mellitus on In Vivo Insulin-stimulated Glucose Utilization , 1984, Diabetes.

[9]  J. A. Scarlett,et al.  The Acute and Chronic Effects of Sulfonylurea Therapy in Type II Diabetic Subjects , 1984, Diabetes.

[10]  R. DeFronzo,et al.  Mechanism of improvement in glucose metabolism after chronic glyburide therapy. , 1984, Diabetes.

[11]  G. Reaven,et al.  Insulin secretion and action in noninsulin-dependent diabetes mellitus. Is insulin resistance secondary to hypoinsulinemia? , 1983, The American journal of medicine.

[12]  H. Ginsberg,et al.  Effect of Insulin Therapy on Insulin Resistance in Type II Diabetic Subjects: Evidence for Heterogeneity , 1981, Diabetes.

[13]  C. Glueck,et al.  Plasma High‐density Lipoprotein Cholesterol Comparisons in Black and White Populations: The Lipid Research Clinics Program Prevalence Study , 1980, Circulation.

[14]  J. Olefsky,et al.  Mechanisms of insulin resistance in human obesity: evidence for receptor and postreceptor defects. , 1980, The Journal of clinical investigation.

[15]  R. DeFronzo,et al.  Glucose clamp technique: a method for quantifying insulin secretion and resistance. , 1979, The American journal of physiology.

[16]  J. E. Pinney,et al.  Multilayer film elements for clinical analysis: general concepts. , 1978, Clinical chemistry.

[17]  R. Schifman,et al.  Cholesterol in high-density lipoprotein: use of Mg2+/dextran sulfate in its enzymic measurement. , 1978, Clinical chemistry.

[18]  G. Miller,et al.  Inverse relationship in Jamaica between plasma high-density lipoprotein cholesterol concentration and coronary-disease risk as predicted by multiple risk-factor status. , 1976, Clinical science and molecular medicine.

[19]  E. Bernt,et al.  Enzymatic determination of total cholesterol in serum. , 1974, Zeitschrift fur klinische Chemie und klinische Biochemie.

[20]  M Berman,et al.  A model of the kinetics of insulin in man. , 1974, The Journal of clinical investigation.

[21]  P. Fu,et al.  Enzymatic determination of total serum cholesterol. , 1974, Clinical chemistry.

[22]  R. Levy,et al.  Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. , 1972, Clinical chemistry.

[23]  A. Lazarow,et al.  Immunoassay of Insulin: Two Antibody System: Plasma Insulin Levels of Normal, Subdiabetic and Diabetic Rats , 1963, Diabetes.

[24]  R. Steele,et al.  INFLUENCES OF GLUCOSE LOADING AND OF INJECTED INSULIN ON HEPATIC GLUCOSE OUTPUT * , 1959, Annals of the New York Academy of Sciences.

[25]  J. Haldane.  Simple tests for bimodality and bitangentiality. , 1952, Annals of eugenics.