A substantial proportion of adrenal incidentalomas demonstrates subtle hormonal hypersecretion; however, adenomas that cosecrete aldosterone and cortisol are rare. We here report a case of an adrenal mass that was incidentally detected on a computed tomography scan in a 57-year-old man. The patient had a 10-year history of diabetes mellitus and a 5-year history of hypertension. Evaluation revealed hyperaldosteronemia with an elevated plasma aldosterone-to-renin ratio, hypokalemia, unsuppressed cortisol after dexamethasone administration, and elevated urinary free cortisol concentration. The appearance of the right adrenalectomy specimen indicated adrenal adenoma. Postoperatively, the blood glucose and blood pressure control improved and the urinary cortisol and aldosterone-to-renin ratio normalized. A complete endocrine evaluation in patients with incidentally discovered adrenal masses should be performed, even if the patient has a long-standing history of hypertension and diabetes, to avoid any postoperative adrenal crises.
Diabetic patients develop hypoaldosteronism which frequently caused hyperkalemia and metabolic acidosis and diabetic hypoaldosteronism is associated with selective unresponsiveness of aldosterone to angiotensin II(A II), but mechanism of defect in A II stimulated aldosterone response still remain unclear.
To elucidate the mechanism of defect in A II stimulated aldosterone response and whether the defect was corrected by insulin treatment. author evaluated the responses of aldosterone production to A II, K+ and ACTH. I also evaluated the products of phospholipase C(PLC) and phospholipase D(PLD) activation important for increase of intracellular calcium and protein kinase C activation after A II activation in adrenal glomerulosa cells prepared from streptozotocin induced diabetic rats.
Two weeks after induction of diabetes by streptozotocin, rats were sacrificed by decapitation. The aldosterone production to A II, K+ and ACTH was measured by RIA. Inositol triphosphate(IP3) and diacylglycerol(DAG) generated by activation of PLC and phosphatidic acid(PA), phosphatidylethanol(PEt) and DAG generated by activation of PLD were measured by anion exchange column and thin layer chromatography.
1) Plasma renin activity and aldosterone level were not different among control rats, untreated and insulin treated diabetic rats.
2) basal, ACTH and K+-stimulated aldosterone production were similar in cells from the three groups(p>0.05), but A II stimulated aldosterone production was significantly decreased in cells from untreated diabetic rats compared with control and insulin treated diabetic rats(p<0.05).
3) A II-induced IP3, PA, PEt and DAG generation was similar among the three groups(p>0.05).
These results suggested that decreased A II-stimulated aldosterone response was present in glomerulosa cells from strepzptocin induced diabetic rats and reversed by insulin treatments. The main defect of altered A II response of zona glomerulosa might be located in the step distal to the activation of phospholipase.
Gestational diabetes mellitus (GDM) affects 2%-4% of the all pregnant women, and it is a major risk factor for development of type 2 DM. We performed this cross-sectional study to determine whether there were defects in insulin secretory capacity or insulin sensitivity in women with previous GDM.
On 6-8 weeks after delivery, 75 g oral glucose tolerance test was performed in 36 women with previous GDM and 19 non-pregnant control women matched with age and weight. Intravenous glucose tolerance test was performed on 10-14 weeks after delivery. Insulin secretory capacity measured as the acute insulin response to glucose (AIRg) and insulin sensitivity as minimal model derived sensitivity index (SI) were obtained. AIRg×SI (β-cell disposition index) was used as an index of β-cell function.
Women with previous GDM were classified into normal glucose tolerance (postpartum-NGT, n=19) and impaired glucose tolerance (postpartum-IGT, n=17). Postpartum fasting glucose levels were significantly higher in postpartum-IGT compared to postpartum-NGT and control (P<0.05). AIRg×SI was significantly lower in postpartum-IGT compared to control (P<0.05). SI was lower in postpartum-NGT and postpartum-IGT compared to control, but the difference did not have the statistical significance. Frequency of parental history of type 2 diabetes was significantly greater in postpartum-IGT compared to postpartum-NGT (P<0.05).
Women with previous GDM showed impaired insulin secretion although their glucose tolerance states were restored to normal. It suggests impaired early insulin secretion may be a major pathophysiologic factor for development of type 2 DM, and this defect may be genetically determined.
Insulin resistance is a major pathophysiology in polycystic ovary syndrome (PCOS), and assessment of insulin sensitivity is important. Various insulin sensitivity indices from fasting state or oral glucose tolerance test (OGTT) have been compared with euglycemic hyperinsulinemic clamp. We aimed to evaluate the usefulness of these indices in young Korean women with PCOS.
Euglycemic hyperinsulinemic clamp test and 75 g OGTT were performed in 290 women with PCOS. Insulin mediated glucose uptake (IMGU), the insulin sensitivity index from clamp, was compared with various insulin sensitivity indices such as composite insulin sensitivity index (ISIcomp), estimated metabolic clearance rate (MCRest) of glucose and estimated insulin sensitivity index (ISIest), area under the curve of glucose and insulin ratio (AUC-GIR), OGTT-derived Belfiore index, and oral glucose insulin sensitivity index (OGSI) by Kazama. Fasting state indices such as glucose insulin ratio (GIR), homeostasis model assessment for insulin resistance (HOMA-IR), fasting Belfiore index, and quantitative insulin sensitivity check index (QUICKI) were also compared with IMGU.
The correlation coefficients of ISIcomp, MCRest, ISIest, AUC-GIR, OGTT-Belfiore index, and OGSI with IMGU were all about 0.5 (Ps'<0.001) in PCOS women as a whole. The MCRest and ISIest were significantly correlated with IMGU in both obese (r=0.58 and 0.58, P<0.0001) and non-obese subjects (r=0.33 and 0.32, P<0.001). Fasting glucose and insulin-derived indices showed worse correlation with IMGU than OGTT-derived ones.
The MCRest and ISIest from OGTT might be the best replacement for the insulin sensitivity index from hyperinsulinemic euglycemic clamp independent of obesity.
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