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      Glucose tolerance and insulin responsiveness in Gitelman syndrome patients

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          Abstract

          Objective

          Impaired glucose metabolism and insulin sensitivity have been reported in patients with Gitelman syndrome (GS), but insulin secretion and the related mechanisms are not well understood.

          Design and methods

          The serum glucose levels, insulin secretion and insulin sensitivity were evaluated in patients with GS ( n = 28), patients with type 2 diabetes mellitus (DM) and healthy individuals ( n = 20 in both groups) using an oral glucose tolerance test. Serum and urine sodium, potassium and creatinine levels were measured at 0, 30, 60, 120 and 180 min after an oral glucose load was administered.

          Results

          The areas under the serum glucose curves were higher in the GS patients than those in the healthy controls (17.4 ± 5.1 mmol·h/L vs 14.5 ± 2.8 mmol·h/L, P = 0.02) but lower than those in the DM patients (24.8 ± 5.3 mmol·h/L, P < 0.001). The areas under the serum insulin curves and the insulin secretion indexes in GS patients were higher than those in DM patients and lower than those in healthy subjects. The insulin secretion-sensitivity index of GS patients was between that of healthy subjects and DM patients, but the insulin sensitivity indices were not different among the three groups. After one hour of glucose administration, the serum potassium level significantly decreased from baseline, and the urinary potassium-to-creatinine ratio increased gradually and peaked at 2 h.

          Conclusions

          Glucose metabolism and insulin secretion were impaired in GS patients, but insulin sensitivity was comparable between GS patients and patients with type 2 DM. After administration of an oral glucose load, the plasma potassium level decreased in GS patients due to the increased excretion of potassium in the urine.

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          Most cited references19

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          Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans.

          Insulin resistance plays an important role in the pathophysiology of diabetes and is associated with obesity and other cardiovascular risk factors. The "gold standard" glucose clamp and minimal model analysis are two established methods for determining insulin sensitivity in vivo, but neither is easily implemented in large studies. Thus, it is of interest to develop a simple, accurate method for assessing insulin sensitivity that is useful for clinical investigations. We performed both hyperinsulinemic isoglycemic glucose clamp and insulin-modified frequently sampled iv glucose tolerance tests on 28 nonobese, 13 obese, and 15 type 2 diabetic subjects. We obtained correlations between indexes of insulin sensitivity from glucose clamp studies (SI(Clamp)) and minimal model analysis (SI(MM)) that were comparable to previous reports (r = 0.57). We performed a sensitivity analysis on our data and discovered that physiological steady state values [i.e. fasting insulin (I(0)) and glucose (G(0))] contain critical information about insulin sensitivity. We defined a quantitative insulin sensitivity check index (QUICKI = 1/[log(I(0)) + log(G(0))]) that has substantially better correlation with SI(Clamp) (r = 0.78) than the correlation we observed between SI(MM) and SI(Clamp). Moreover, we observed a comparable overall correlation between QUICKI and SI(Clamp) in a totally independent group of 21 obese and 14 nonobese subjects from another institution. We conclude that QUICKI is an index of insulin sensitivity obtained from a fasting blood sample that may be useful for clinical research.
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            Oral glucose tolerance test indexes for insulin sensitivity and secretion based on various availabilities of sampling times.

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              Dietary calcium and magnesium, major food sources, and risk of type 2 diabetes in U.S. black women.

              Inverse associations between magnesium and calcium intakes and risk of type 2 diabetes have been reported for studies in predominantly white populations. We examined magnesium, calcium, and major food sources in relation to type 2 diabetes in African-American women. This is a prospective cohort study including 41,186 participants of the Black Women's Health Study without a history of diabetes who completed validated food frequency questionnaires at baseline. During 8 years of follow-up (1995-2003), we documented 1,964 newly diagnosed cases of type 2 diabetes. The multivariate-adjusted hazard ratio of type 2 diabetes for the highest compared with the lowest quintile of intake was 0.69 (95% CI 0.59-0.81; P trend <0.0001) for dietary magnesium and 0.86 (0.74-1.00; P trend = 0.01) for dietary calcium. After mutual adjustment, the association for calcium disappeared (hazard ratio 1.04 [95% CI 0.88-1.24]; P trend = 0.88), whereas the association for magnesium remained. Daily consumption of low-fat dairy (0.87 [0.76-1.00]; P trend = 0.04) and whole grains (0.69 [0.60-0.79]; P trend <0.0001) were associated with a lower risk of type 2 diabetes compared with a consumption less than once a week. After mutual adjustment, the hazard ratio was 0.81 (0.68-0.97; P trend = 0.02) for magnesium and 0.73 (0.63-0.85; P trend <0.0001) for whole grains. These findings indicate that a diet high in magnesium-rich foods, particularly whole grains, is associated with a substantially lower risk of type 2 diabetes in U.S. black women.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                May 2017
                21 April 2017
                : 6
                : 4
                : 243-252
                Affiliations
                [1 ]Department of Endocrinology & Key Laboratory of Endocrinology The National Health and Family Planning Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China
                [2 ]Department of Nephrology Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China
                [3 ]Department of Pediatrics State Key Laboratory of Medical Genetics, Xiangya Hospital, Central South University, Changsha, China
                Author notes
                Correspondence should be addressed to L Chen or X Xing; Email: chenlimeng@ 123456pumch.cn or xingxp2006@ 123456126.com
                [*]

                (T Yuan and L Jiang contributed equally to this work)

                Article
                EC170014
                10.1530/EC-17-0014
                5632718
                28432081
                21f5ed70-77f7-4726-8a50-9abff7249a54
                © 2017 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 7 April 2017
                : 21 April 2017
                Categories
                Research

                gitelman syndrome,glucose metabolism,insulin secretion,insulin resistance

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