Differences in the in vivo insulin secretion and sensitivity of healthy black versus white adolescents

Arslanian, Silva; Suprasongsin, Chittiwat

doi:10.1016/s0022-3476(96)70078-1

Cited by 177 publications

(148 citation statements)

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“…Conversely, Jiang et al, 7 in a biracial sample of 1157 adolescents from the Bogalusa Heart Study, reported that the higher insulin concentration in AAs was mainly explained by reduced hepatic insulin clearance as determined by a lower C-peptide/insulin ratio. Arslanian et al, 8 suggested that the higher insulin secretion in AAs (50% first-phase and 38% second phase) represented a compensatory mechanism to overcome the 35% decrease in insulin sensitivity. In agreement with these reports, our study indicates that at comparable levels of insulin sensitivity, obese AAs have higher b-cell activity and impaired insulin clearance compared to obese C. A novel finding in this study is that at similar levels of glucose, BMI, fat mass (DEXA, WHR, leptin), dietary intake, and insulin sensitivity, obese AAs have significantly higher fasting and stimulated GLP-1 concentrations than obese C. Changes in GLP-1 levels paralleled changes in b-cell activity (CIR 30 ) and preceded the peak insulin response during the OGTT.…”

Section: Discussionmentioning

confidence: 99%

“…5,6 Several studies have reported increased b-cell activity as the primary mechanism for this hyperinsulinemic state in black patients; 6 while others, have suggested that the hyperinsulinemia is the result of decreased hepatic insulin clearance 7 and reduced insulin sensitivity. 8 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide gastric inhibitory polypeptide (GIP) are the two most important incretins. 9 In humans, GLP-1 results from post-translational processing of proglucagon in the intestinal L-cells and accounts for 80% of the intestinal incretin effect.…”

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confidence: 99%

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Racial differences in glucagon-like peptide-1 (GLP-1) concentrations and insulin dynamics during oral glucose tolerance test in obese subjects

et al. 2003

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Obese African-American (AA) subjects have higher resting and stimulated insulin concentrations than obese Caucasians (C), which could not be explained by the severity of obesity or the degree of insulin sensitivity. We investigated whether differences in glucagon-like peptide-1 (GLP-1), the most potent incretin that regulates insulin secretion, might explain racial differences in insulin response. Accordingly, we measured fasting and stimulated glucose, insulin, and GLP-1 levels during a 3-h oral glucose tolerance test (OGTT) in 26 obese C (age 3872 y, body mass index 4471 kg/m 2 ) and 16 obese AA (age 3672 y, BMI 4672 kg/ m 2 ) subjects. Corrected insulin response (CIR 30 ), a measure of b-cell activity, whole body insulin sensitivity index (WBISI), and area under the curve (AUC) for insulin, GLP-1, and C-peptide/insulin ratio were computed from the OGTT. Glucose levels, fasting and during the OGTT, were similar between racial groups; 32% of the C and 31% of the AA subjects had impaired glucose tolerance. Keywords: GLP-1; insulin; racial; b-cell activity Obesity is characterized by hyperinsulinemia and increased insulin resistance. 1 Several in vitro and in vivo studies have shown that hyperinsulinemia may play an important role in the pathogenesis of obesity through regulation of appetite, fat cell metabolism, and energy expenditure. 2-4 Recent different cross-sectional and longitudinal studies have reported that both lean and obese African Americans (AA) exhibit higher fasting and stimulated insulin levels when compared with their white counterparts. 5,6 Several studies have reported increased b-cell activity as the primary mechanism for this hyperinsulinemic state in black patients; 6 while others, have suggested that the hyperinsulinemia is the result of decreased hepatic insulin clearance 7 and reduced insulin sensitivity. 8 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide gastric inhibitory polypeptide (GIP) are the two most important incretins. 9 In humans, GLP-1 results from post-translational processing of proglucagon in the intestinal L-cells and accounts for 80% of the intestinal incretin effect. 10 GLP-1's action is mediated by its binding to cell surface receptors (GLP-1R) that are highly expressed on the cell membranes of pancreatic b-cells. 10,11 In addition to stimulating insulin secretion, GLP-1 has been shown to have other profound biological effects on b-cells. 12 GLP-1 regulates b-cell function by maintaining a portion of the b-cell population in a glucose-competent state by making resistant islets glucose sensitive. [13][14][15][16] Recent evidence suggests that GLP-1 may also promote regeneration of islet cells and expansion of the b-cell mass. 12,17 Racial differences in GLP-1 concentrations in obese subjects have not been previously reported. Based on GLP-

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Racial differences in glucagon-like peptide-1 (GLP-1) concentrations and insulin dynamics during oral glucose tolerance test in obese subjects

et al. 2003

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“…e and others have demonstrated that AfricanAmerican (AA) children are hyperinsulinemic compared with their American white (AW) peers (1)(2)(3)(4). This hyperinsulinemia has typically been explained as a compensatory adaptation to low insulin sensitivity in AAs (2)(3)(4).…”

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confidence: 99%

“…This hyperinsulinemia has typically been explained as a compensatory adaptation to low insulin sensitivity in AAs (2)(3)(4). However, another explanation is decreased insulin clearance based on the observation of lower C-peptide to insulin ratios in AA adolescents and adults compared with AWs (5,6).…”

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confidence: 99%

Hyperinsulinemia in African-American Children

et al. 2002

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African-American (AA) children are hyperinsulinemic and insulin resistant compared with American White (AW) children. This study investigated 1) whether AA/AW differences in insulinemia are associated with differences in insulin clearance; 2) whether dietary patterns, mainly carbohydrate and fat intake, play a role; and 3) whether the quantitative relationship between insulin sensitivity and secretion is similar between AA and AW children. Forty-four prepubertal children (22 AA and 22 AW) with comparable body composition and visceral adiposity were studied. All underwent a 3-h hyperinsulinemic (40 mU ⅐ m ؊2 ⅐ min ؊1)-euglycemic clamp to calculate insulin sensitivity and insulin clearance and a 2-h hyperglycemic clamp (12.5 mmol/l) to assess first-and second-phase insulin responses. Twenty-four-hour food recalls were analyzed for macronutrient intake. Insulin clearance (19.5 ؎ 0.7 vs. 22.9 ؎ 1.1 ml ⅐ min ؊1 ⅐ kg ؊1 fat-free mass [FFM]; P ‫؍‬ 0.011) and insulin sensitivity were lower in AA versus AW children (14.8 ؎ 1.0 vs. 18.9 ؎ 1.4 mol ⅐ min ؊1 ⅐ kg ؊1 FFM; P ‫؍‬ 0.021). Both insulin clearance and insulin sensitivity correlated inversely with dietary fat/carbohydrate ratio, which was higher in AA than in white children. Fasting C-peptide and insulin were higher in AA children with no difference in proinsulin levels. First-and second-phase insulin concentrations and glucose disposition index (insulin sensitivity ؋ first-phase insulin) were higher in AA than in white children (12.8 ؎ 2.1 vs. 7.2 ؎ 0.6 mol ⅐ min ؊1 ⅐ kg ؊1 FFM; P ‫؍‬ 0.019). In conclusion, the hyperinsulinemia observed in AA children is due to both lower insulin clearance and higher insulin secretion compared with their white peers. The quantitative relationship between insulin secretion and sensitivity is upregulated in AA children. This suggests that increased insulin secretion in AA children is not merely a compensatory response to lower insulin sensitivity. Dietary factors may have a role. Additional studies are needed to determine whether metabolic/nutritional factors, possibly mediated through free fatty acids, may play a role in the hyperinsulinism observed in AA children. Diabetes 51:3014 -3019, 2002

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“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14] Although much of the literature reflects a higher risk for obesity and type 2 diabetes in ethnic populations such as American Indians, African Americans, Hispanics, Asians, and South Pacific Islanders (all of whom are considered genetically predisposed for insulin resistance), the incidence is rising in all population groups.…”

Section: Clinical Decision Makingmentioning

confidence: 99%

Recognizing the Signs of Metabolic Syndrome and Polycystic Ovary Syndrome in a Caucasian Adolescent Girl: Differentiating Type 2 From Type 1 Diabetes

Murray¹

2002

Diabetes Spectrum

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Differences in the in vivo insulin secretion and sensitivity of healthy black versus white adolescents

Cited by 177 publications

References 11 publications

Racial differences in glucagon-like peptide-1 (GLP-1) concentrations and insulin dynamics during oral glucose tolerance test in obese subjects

Racial differences in glucagon-like peptide-1 (GLP-1) concentrations and insulin dynamics during oral glucose tolerance test in obese subjects

Hyperinsulinemia in African-American Children

Recognizing the Signs of Metabolic Syndrome and Polycystic Ovary Syndrome in a Caucasian Adolescent Girl: Differentiating Type 2 From Type 1 Diabetes

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