Beta-cell Function In Women Research Articles

Possible mechanisms involved in improved beta cell function in pregnant women with type 1 diabetes

Pregnancy is known to be associated with an increased demand for insulin that is normally compensated by an increased beta cell mass and insulin secretion. Recent studies have suggested enhanced beta cell function during pregnancy in women with type 1 diabetes (T1D). To explore the possible mechanisms behind enhanced beta cell function during pregnancy in women with T1D we investigated the impact of circulating factors in serum from nine women from each group of pregnant women with and without T1D, after pregnancy and non-diabetic non-pregnant women on rat islet cell proliferation and apoptosis, and on T-lymphocyte activation. In addition, circulating levels of pancreatic hormones and selected cytokines and adipokines were measured. Rat islet cell proliferation was higher in serum from pregnant women with T1D (p < 0.05) compared to T1D women after pregnancy. Apoptosis in INS-1E cell was lower (p < 0.05) in serum from pregnant women with T1D compared to T1D women after pregnancy. T-lymphocyte cell (Jurkat) proliferation was reduced by serum from pregnant women without T1D only (p < 0.05). Higher C-peptide levels and lower levels of ghrelin, IL-6, MCP-1, IL-8 and adipsin were observed in pregnant women with T1D compared to T1D women after pregnancy. In conclusion, the improved beta cell function in women with T1D during pregnancy may be due to lower levels of proinflammatory cytokines and/or higher levels of pregnancy-associated growth factors.

Pancreatic fat deposition is increased and related to beta-cell function in women with familial partial lipodystrophy

BackgroundTo study pancreatic fat deposition and beta-cell function in familial partial lipodystrophy (FPLD) patients.MethodsIn a cross-sectional study, eleven patients with FPLD, and eight healthy volunteers were matched for age and body mass index and studied at a referral center. Body composition was assessed using dual-energy X-ray absorptiometry and the Dixon method of magnetic resonance imaging was used to quantify pancreatic and liver fat. Fasting plasma glucose, insulin, leptin, lipids and homeostasis model assessment of insulin resistance values were measured, and an oral glucose tolerance test was performed. The insulinogenic index, Matsuda insulin sensitivity index and beta-cell disposition index were calculated.ResultsThe FPLD group presented a higher waist-to-hip ratio and fat mass ratio and lower total, truncal and lower-limb fat masses. Pancreatic and liver fat contents (log transformed) were significantly higher in the FPLD group (5.26 ± 1.5 vs. 4.08 ± 0.64, p = 0.034 and 0.77 ± 0.50 vs. 0.41 ± 0.18, p = 0.056, respectively). Pancreatic fat was inversely related to the DI (r = − 0.53, p = 0.027) and HDL-cholesterol (r = − 0.63, p = 0.003) and directly related to WHR (r = 0.60; p = 0.009), HbA1c (r = 0.58; p = 0.01) and serum triglyceride (r = 0.48, p = 0.034). Higher triglyceride and lower HDL-cholesterol levels were observed in the FPLD group.ConclusionsThis study demonstrated for the first time that pancreatic fat deposition is increased in FPLD. Moreover, an inverse relationship was demonstrated between pancreatic fat and beta-cell function. The findings of this study may be consistent with the expandability hypothesis and the twin cycle hypothesis.

Serum concentrations of betatrophin and its association with indirect indices of insulin resistance and beta cell function in women with polycystic ovary syndrome

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Serum Concentrations of Betatrophin and Its Association with Indirect Indices of Insulin Resistance and Beta Cell Function in Women with Polycystic Ovary Syndrome.

Introduction Data underline the role of betatrophin in glucose homeostasis. Polycystic ovary syndrome (PCOS) is characterized by insulin resistance (IR). The aim of our study was to investigate the relationship of serum betatrophin concentrations with indirect indices of IR and insulin secretion in women with PCOS, compared to the control group. Methods The study group comprised 43 women with PCOS and 16 controls. IR was assessed by HOMA-IR and Matsuda index. Insulin secretion was evaluated with HOMA-B. An oral glucose tolerance test (OGTT) with estimation of serum betatrophin concentrations was performed. Results Glucose load resulted in an increase in serum betatrophin concentrations in the control group (p = 0.02). Serum betatrophin concentrations at 120 min of OGTT were lower in women with PCOS than in the control group (p = 0.02). We observed positive correlations between baseline serum betatrophin concentrations and HOMA-IR (r = 0.39, p = 0.008), negative correlations with Matsuda index (r = −0.31, p = 0.004), and a positive relationship with HOMA-B (r = 0.38, p = 0.01) in women with PCOS. Multiple regression analysis revealed that HOMA-B (β = 0.47, p = 0.001) was an independent factor connected to serum betatrophin levels in PCOS. Conclusions Serum concentrations of betatrophin are connected with insulin resistance and beta cell function and did not change after glucose load in women with PCOS.

Evaluation of Circulating Determinants of Beta-Cell Function in Women With and Without Gestational Diabetes.

Gestational diabetes (GDM) arises in women in whom there is insufficient β-cell compensation for the insulin resistance of late pregnancy. The mechanisms underlying both normal antepartum β-cell adaptation and its aberrancy in GDM are unclear. Preclinical studies have suggested that the hormones prolactin and human placental lactogen (HPL) may stimulate β-cell mass, whereas the furan fatty acid metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) has recently emerged as a potential negative regulator of β-cell function. However, there has been limited study of these factors in humans. Our objective was to systematically evaluate HPL, prolactin, and CMPF in relation to glucose homeostasis and β-cell function in women with and without GDM. Three-hundred-and-ninety-five women underwent an oral glucose tolerance test in late pregnancy, enabling assessment of GDM status, glycemia (area-under-the-glucose-curve on oral glucose tolerance test [AUCglucose]), β-cell function (Insulin Secretion-Sensitivity Index-2, insulinogenic index/homeostatic model assessment of insulin resistance [HOMA-IR]), insulin sensitivity/resistance (Matsuda index, HOMA-IR), and circulating HPL, prolactin, and CMPF. Serum concentrations of HPL, prolactin, and CMPF were similar between women with GDM (n = 105) and women without GDM (n = 290). However, on multiple linear regression analyses, CMPF emerged as a significant predictor of AUCglucose in women with GDM (t = 4.75, P < .0001) but not in their peers (P = .60). Furthermore, CMPF independently predicted lower Insulin Secretion-Sensitivity Index-2 (t = -2.28, P = .02) and lower insulinogenic index/HOMA-IR (t = -2.22, P = .03) in women with GDM but not in the non-GDM group (both P = .93). Neither HPL nor prolactin was significantly associated with AUCglucose, β-cell function, or insulin sensitivity. CMPF is a potential circulating determinant of β-cell dysfunction and hyperglycemia in women with GDM.

The insulin secretion-sensitivity index-2 (ISSI-2) and the measurement of beta-cell function in women with gestational diabetes

The insulin secretion-sensitivity index-2 (ISSI-2) and the measurement of beta-cell function in women with gestational diabetes

Plasma relaxin concentration is related to beta-cell function and insulin sensitivity in women with type 2 diabetes mellitus

We conducted a study to examine an association between relaxin, insulin sensitivity and beta-cell function in women with type 2 diabetes. Relaxin concentration was measured in plasma in 63 newly diagnosed women with type 2 diabetes. We also measured body mass index (BMI), blood pressure, parameters of metabolic control (fasting glucose level, HbA1c, total, HDL and LDL cholesterol, triglycerides) and insulin resistance according to the homeostasis model assessment index 2 (HOMA2). Relaxin was positively related to insulin sensitivity ( R = 0.316 and p = 0.01) and negatively to beta-cell (−0.382 and p = 0.004) function. Logistic regression analysis revealed that the correlation between relaxin and HOMA2%B remained significant after adjustment for age, BMI ( R 2 = 0.253 and p = 0.006). Our data raise the possibility that a gender-related hormonal mechanism may influence beta-cell function in women with type 2 diabetes.

P-853: Hyperproinsulinemia, insulin resistance and Beta-cell function in women with polycystic ovary syndrome

P-853: Hyperproinsulinemia, insulin resistance and Beta-cell function in women with polycystic ovary syndrome

Effect of troglitazone on insulin sensitivity and pancreatic beta-cell function in women at high risk for NIDDM

Effect of troglitazone on insulin sensitivity and pancreatic beta-cell function in women at high risk for NIDDM

Decreased beta-cell function in women with previous small for gestational age infants.

Insulin, proinsulin and C-peptide responses to intravenous glucose (glucose infusion test, GIT) and insulin sensitivity were measured in women who previously and for unexplained reasons gave birth to small-for-gestational-age infants (SGA, n = 10) or appropriate-for-gestational-age infants (AGA, n = 11). Insulin sensitivity was evaluated by two different methods, somatostatin-, insulin- and glucose infusion test (SIGIT) and Bergman's minimal model method applied to the frequently samples intravenous glucose tolerance test. The two groups were comparable with regard to age, parity and body mass index. The SGA group exhibited significantly (p < 0.01) lower early (0-10 min) and late (10-60 min) insulin, C-peptide and proinsulin responses during GIT than were seen in the control AGA group. Insulin sensitivity evaluated by the two techniques was increased in the SGA group, significantly so only with the minimal model method. The insulin sensitivity index (Si) according to Bergman was 10.98 +/- 2.10 in the SGA as compared to 4.36 +/- 1.18 x 10(-4)min-1 x uU-1 in the AGA group (antilogged values +/- 95% confidence intervals). Early insulin response (GIT) and Si values were inversely correlated (r = -0.48, p < 0.05).