β-Cell tropin, the pituitary peptide ACTH22–39, is a potent insulin secretagogue and stimulates lipogenesis in adipose tissue in rodents. Plasma β-cell tropin was measured fasting and after glucose infusion (5 mg · kg glucose ideal body weight−1 · min−1 for 90 min) in 10 mild diet-treated non-insulin-dependent (type II) diabetic subjects and 10 control subjects (body mass index) (BMI): 26.4 ± 3.2 and 24.1 ± 2.0 kg/m−2, NS, fasting plasma glucose 7.8 ± 2.7 mM and 4.7 ± 0.3 mM, respectively). The diabetic subjects had raised fasting plasma β-cell tropin compared with the normal subjects (geometric mean (1 SD range): 0.49 (0.25–0.96) nM and 0.17 (0.10–0.28) nM, respectively, P = 0.007). In response to the glucose infusion, plasma glucose rose higher in the diabetic subjects (mean ± 1 SD: 13.7 ± 3.1 and 9.6 ± 0.9 mM, P = 0.007) and plasma insulin was impaired in the diabetic compared with the nondiabetic subjects (geometric mean (1 SD range): 14 (8–26) and 34 (18–63), P <0.01). β-Cell tropin concentrations in the diabetic subjects rose to 1.31 (0.74–2.30) nM (P = 0.007), whereas β-cell tropin did not change in the normal subjects at 0.19 (0.11–0.91) nM. There was no overlap between glucose-stimulated plasma β-cell tropin in the two groups (P = 0.0002). Pituitary-adrenal function, as assessed by plasma cortisol, did not differ between the two groups when fasting and did not change after the glucose infusion. Though its physiological role is unclear, abnormal plasma β-cell tropin may be a feature of type II diabetes.

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