6 research outputs found

    Growth hormone receptor regulates β cell hyperplasia and glucose-stimulated insulin secretion in obese mice

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    Insulin, growth hormone (GH), and insulin-like growth factor–1 (IGF-1) play key roles in the regulation of β cell growth and function. Although β cells express the GH receptor, the direct effects of GH on β cells remain largely unknown. Here we have employed a rat insulin II promoter–driven (RIP-driven) Cre recombinase to disrupt the GH receptor in β cells (βGHRKO). βGHRKO mice fed a standard chow diet exhibited impaired glucose-stimulated insulin secretion but had no changes in β cell mass. When challenged with a high-fat diet, βGHRKO mice showed evidence of a β cell secretory defect, with further deterioration of glucose homeostasis indicated by their altered glucose tolerance and blunted glucose-stimulated insulin secretion. Interestingly, βGHRKO mice were impaired in β cell hyperplasia in response to a high-fat diet, with decreased β cell proliferation and overall reduced β cell mass. Therefore, GH receptor plays critical roles in glucose-stimulated insulin secretion and β cell compensation in response to a high-fat diet

    Disparities in the Prescription of Statins in the Primary Care Setting: A Retrospective Observational Study.

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    Despite the high disease burden of atherosclerosis, evidence exists for the disparity in the prescription of guideline-indicated medications between genders, racial groups, socioeconomic groups, and ages. We aim to perform a retrospective study looking at the disparity in statin prescription for primary and secondary prevention in these groups. Data were collected from a single center and included patients with an LDL level \u3e190 mg/dL, diagnosis of diabetes mellitus with LDL level \u3e70 mg/dL, and diagnosis of cardiovascular disease regardless of LDL level. Patients older than 75 or younger than 21 were excluded from the study. Complex samples multivariable logistic and linear regression models were used to calculate the adjusted odds ratio and 95% confidence interval. The total study population was n = 56,995. Of those, 57.89% (n = 32,992) were female. Only 59.56 % of these patients for whom statin therapy was indicated received it. Most patients were White (53.21%) followed by African Americans (35.98%), Asians (2.43%), American Indian/Native Alaskans (0.40%), and Native Hawaiian/Pacific Islander (0.18%). There is a clear disparity in statin prescription favoring males, the elderly, and people of white ethnicity. Interestingly, Asians were more likely to be prescribed statins as opposed to whites. Self-pay patients were more likely to receive statins than patients on Medicare.Despite being indicated, Statins are under prescribed. Disparities based on race, gender, and insurance type mirror previous trends in the literature. Some results have shown a reversal in trends such as the higher prescription for Asian-Americans. Multiple patient-specific, provider-related, institutional factors might explain these disparities and must be investigated

    Characterization of Erg K+ Channels in α- and β-Cells of Mouse and Human Islets*

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    Voltage-gated eag-related gene (Erg) K+ channels regulate the electrical activity of many cell types. Data regarding Erg channel expression and function in electrically excitable glucagon and insulin producing cells of the pancreas is limited. In the present study Erg1 mRNA and protein were shown to be highly expressed in human and mouse islets and in α-TC6 and Min6 cells α- and β-cell lines, respectively. Whole cell patch clamp recordings demonstrated the functional expression of Erg1 in α- and β-cells, with rBeKm1, an Erg1 antagonist, blocking inward tail currents elicited by a double pulse protocol. Additionally, a small interference RNA approach targeting the kcnh2 gene (Erg1) induced a significant decrease of Erg1 inward tail current in Min6 cells. To investigate further the role of Erg channels in mouse and human islets, ratiometric Fura-2 AM Ca2+-imaging experiments were performed on isolated α- and β-cells. Blocking Erg channels with rBeKm1 induced a transient cytoplasmic Ca2+ increase in both α- and β-cells. This resulted in an increased glucose-dependent insulin secretion, but conversely impaired glucagon secretion under low glucose conditions. Together, these data present Erg1 channels as new mediators of α- and β-cell repolarization. However, antagonism of Erg1 has divergent effects in these cells; to augment glucose-dependent insulin secretion and inhibit low glucose stimulated glucagon secretion
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