Journal articles: 'Insulin; Diabetes; Hypertension'

1

Axelrod, L. "Insulin, prostaglandins, and the pathogenesis of hypertension." Diabetes 40, no. 10 (October 1, 1991): 1223–27. http://dx.doi.org/10.2337/diabetes.40.10.1223.

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2

Nosadini, R., P. Fioretto, R. Trevisan, and G. Crepaldi. "Insulin-Dependent Diabetes Mellitus and Hypertension." Diabetes Care 14, no. 3 (March 1, 1991): 210–19. http://dx.doi.org/10.2337/diacare.14.3.210.

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3

Yudkin, J. S. "Hypertension and non-insulin dependent diabetes." BMJ 303, no. 6805 (September 28, 1991): 730–32. http://dx.doi.org/10.1136/bmj.303.6805.730.

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4

Walden, R. "Hypertension and non-insulin dependent diabetes." BMJ 303, no. 6809 (October 26, 1991): 1063. http://dx.doi.org/10.1136/bmj.303.6809.1063-b.

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5

Donnelly, R., and J. M. Connell. "Hypertension and non-insulin dependent diabetes." BMJ 303, no. 6810 (November 2, 1991): 1134. http://dx.doi.org/10.1136/bmj.303.6810.1134-a.

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6

Crepaldi, G., A. Carraro, E. Brocco, L. Adezati, D. Andreani, G. Bompiani, P. Brunetti, et al. "Hypertension and non-insulin-dependent diabetes." Acta Diabetologica 32, no. 3 (1995): 203–8. http://dx.doi.org/10.1007/bf00838494.

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7

Sowers, James R. "Insulin resistance and hypertension." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (May 2004): H1597—H1602. http://dx.doi.org/10.1152/ajpheart.00026.2004.

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Diminished insulin (Ins) sensitivity is a characteristic feature of various pathological conditions such as the cardiometabolic syndrome, Type 2 diabetes, and hypertension. Persons with essential hypertension are more prone than normotensive persons to develop diabetes, and this propensity may reflect decreased ability of Ins to promote relaxation and glucose transport in vascular and skeletal muscle tissue, respectively. There are increasing data suggesting that ANG II acting through its ANG type 1 receptor inhibits the actions of Ins in vascular and skeletal muscle tissue, in part, by interfering with Ins signally through phosphatidylinositol 3-kinase (PI3K) and its downstream protein kinase B (Akt) signaling pathways. This inhibitory action of ANG II is mediated, in part, through stimulation of RhoA activity and oxidative stress. Activated RhoA and increased reactive oxygen species inhibition of PI3K/Akt signaling results in decreased endothelial cell production of nitric oxide, increased myosin light chain activation with vasoconstriction, and reduced skeletal muscle glucose transport.

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8

OʼHare, James A. "Insulin, insulin resistance, and hypertension." Current Opinion in Endocrinology and Diabetes 1, no. 1 (January 1994): 147–52. http://dx.doi.org/10.1097/00060793-199400010-00027.

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9

HSUEH, W. "Complicated hypertension patients-diabetes and insulin resistance." American Journal of Hypertension 11, no. 4 (April 1998): 247A. http://dx.doi.org/10.1016/s0895-7061(97)91623-x.

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10

Haffner, S. "Insulin resistance, hypertension and type 2 diabetes." American Journal of Hypertension 13, no. 6 (June 2000): S319. http://dx.doi.org/10.1016/s0895-7061(00)00802-5.

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11

Bell, David S. H. "Hypertension, diabetes, insulin resistance, and postprandial hyperglycemia." Drug Development Research 67, no. 7 (2006): 595–96. http://dx.doi.org/10.1002/ddr.20130.

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12

LAAKSO, M., H. SARLUND, and L. MYKKÄNEN. "Essential hypertension and insulin resistance in non-insulin-dependent diabetes." European Journal of Clinical Investigation 19, no. 6 (December 1989): 518–26. http://dx.doi.org/10.1111/j.1365-2362.1989.tb00269.x.

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13

Jarrett, R. J. "Hypertension in Diabetic Patients and Differences Between Insulin-Dependent Diabetes Mellitus and Non-Insulin-Dependent Diabetes Mellitus." American Journal of Kidney Diseases 13, no. 1 (January 1989): 14–16. http://dx.doi.org/10.1016/s0272-6386(89)80107-6.

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14

Monson, J. P., G. Koios, G. C. Toms, P. G. Kopelman, B. J. Boucher, S. J. W. Evans, and W. L. Alexander. "Relationship between Retinopathy and Glycaemic Control in Insulin-Dependent and Non-Insulin-Dependent Diabetes." Journal of the Royal Society of Medicine 79, no. 5 (May 1986): 274–76. http://dx.doi.org/10.1177/014107688607900506.

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The possible relationship between antecedent diabetic control, as determined by serial glycosylated haemoglobin (HbA1) measurements, and diabetic retinopathy was examined in 40 insulin-dependent and 41 non-insulin-dependent diabetics selected consecutively from our clinic population. Multiple logistic regression analysis demonstrated a significant association between mean HbA1 and prevalence of retinopathy in both groups of patients. This association was independent of duration of diabetes which was also significantly associated with retinopathy prevalence. Hypertension and smoking were not obvious risk factors in this group of patients; an apparent association of hypertension and diabetes was entirely accounted for by a positive relationship between the presence of hypertension and duration of diabetes.

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15

Kawamori, Ryuzo. "Insulin Resistance Seen in Non-Insulin Dependent Diabetes Mellitus and Hypertension." Hypertension Research 19, SupplementI (1996): S61—S64. http://dx.doi.org/10.1291/hypres.19.supplementi_s61.

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16

Barri, Yousri M., Biff F. Palmer, and Venkata S. Ram Venkata S. Ram. "Microalbuminuria, insulin resistance, diabetes, hypertension, and kidney function." Postgraduate Medicine 122, no. 6 (November 15, 2010): 34–45. http://dx.doi.org/10.3810/pgm.2005.12.suppl43.230.

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17

Anderson, Julie, and Albert P. Rocchini. "Hypertension in Individuals with Insulin-Dependent Diabetes Mellitus." Pediatric Clinics of North America 40, no. 1 (February 1993): 93–104. http://dx.doi.org/10.1016/s0031-3955(16)38483-8.

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18

Klein, R. "The incidence of hypertension in insulin-dependent diabetes." Archives of Internal Medicine 156, no. 6 (March 25, 1996): 622–27. http://dx.doi.org/10.1001/archinte.156.6.622.

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19

Klein, Ronald. "The Incidence of Hypertension in Insulin-Dependent Diabetes." Archives of Internal Medicine 156, no. 6 (March 25, 1996): 622. http://dx.doi.org/10.1001/archinte.1996.00440060042005.

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20

Ko, Seung-Hyun, Wenhong Cao, and Zhenqi Liu. "Hypertension Management and Microvascular Insulin Resistance in Diabetes." Current Hypertension Reports 12, no. 4 (June 29, 2010): 243–51. http://dx.doi.org/10.1007/s11906-010-0114-6.

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21

Aviv, A. "The roles of cell Ca2+, protein kinase C and the Na(+)-H+ antiport in the development of hypertension and insulin resistance." Journal of the American Society of Nephrology 3, no. 5 (November 1992): 1049–63. http://dx.doi.org/10.1681/asn.v351049.

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There is evidence that the cytosolic free Ca2+, protein kinase C, and the Na(+)-H+ antiport cross-communicate with one another through positive and negative feedback mechanisms, thereby maintaining cellular Ca2+ and pH homeostasis. This triumvirate may play a role in the development of insulin resistance--a common characteristic of both essential hypertension and non-insulin-dependent diabetes mellitus. Circulating cells from patients with essential hypertension and non-insulin-dependent diabetes mellitus demonstrate elevated cytosolic free Ca2+, increased protein kinase C activity, or both, and these perturbations are associated with augmented activity of the Na(+)-H+ antiport. If present in other cells (e.g., striated muscle cells and adipocytes), these alterations could underlie insulin resistance in essential hypertension and non-insulin-dependent diabetes mellitus.

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22

Viberti, G. C., and K. Earle. "Predisposition to essential hypertension and the development of diabetic nephropathy." Journal of the American Society of Nephrology 3, no. 4 (October 1992): S27. http://dx.doi.org/10.1681/asn.v34s27.

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Only a subset of insulin-dependent diabetic patients are at risk of developing nephropathy. Prospective studies of uncomplicated insulin-dependent diabetic cohorts have shown that a rise in systemic arterial pressure is a concomitant feature of the progression to early nephropathy. The development of hypertension is an integral feature of established nephropathy in diabetes, and its amelioration retards the progression of disease and may improve overall mortality. Family studies have suggested that nondiabetic parents of insulin-dependent diabetic patients with nephropathy have a greater prevalence of hypertension, and in certain groups of non-insulin dependent patients, it has been found that the blood pressure before the onset of diabetes correlates with the development of nephropathy after the onset of diabetes. These results indicate that a propensity to hypertension may be part of the genetic predisposition to nephropathy. This contention is further supported by the finding that a raised erythrocyte sodium-lithium countertransport, a biochemical marker of hypertension and cardiovascular disease whose activity is largely genetically determined, occurs with greater frequency in proteinuric diabetic patients and their nondiabetic parents than in those diabetic patients without nephropathy and their parents. Recent family studies have also shown that a family history of cardiovascular disease significantly increases the risk of nephropathy by up to three-fold in insulin-dependent diabetes. It is suggested that the cardiorenal complications of diabetes mellitus may be linked to reduced insulin sensitivity, which itself is associated with hypertension, raised sodium-lithium countertransport rates, and cardiovascular disease.

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23

Rasoulzadegan, Mohammad Hossein, Hamid Reza Soltani, Masoud Rahmanian, and Nakisa Amid. "Insulin Resistance in Patients with Essential Hypertension Using Homeostatic Model Assessment." Internal Medicine and Medical Investigation Journal 3, no. 3 (September 9, 2018): 104. http://dx.doi.org/10.24200/imminv.v2i4.131.

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Introduction: Insulin resistance has a strong relationship with the incidence of type II diabetes. It also has a direct relationship with other risk factors of diabetes, which together are known as metabolic syndrome. The aim of this study was to investigate the relationship between insulin resistance and hypertension.Materials and Methods: In this historical cohort study, 90 patients were divided into three different groups: those without hypertension, those with controlled hypertension, and those with uncontrolled hypertension. Systolic and diastolic blood pressure, body mass index, and laboratory test results such as cholesterol, triglycerides, low- density lipoprotein, high-density lipoprotein, fasting plasma glucose, and fasting plasma insulin were compared among the three groups. Data were analyzed with t-tests and the analysis of variance test, which were performed using statistical package for the social sciences version 20 software.Results: Age and sex were the same among the three groups; however, BMI, systolic blood pressure, and diastolic blood pressure in the uncontrolled-hypertension group were higher than in the controlled-hypertension and without-hypertension groups (P<0.05). Lipid profile (P<0.05), creatinine (P=0.77), and uric acid (P=0.233) were not significantly different among the groups, although fasting plasma insulin (P=0.012) and homeostatic model assessment of insulin resistance (P=0.038) were significantly higher in the uncontrolled-hypertension group than in the other groups.Conclusion: Homeostasis model assessment of insulin resistance in patients with uncontrolled hypertension was higher than in patients with controlled hypertension and those without hypertension. Therefore, homeostatic model assessment of insulin resistance can be used as a predictive clinical test for the early diagnosis of diabetes in patients with uncontrolled hypertension.

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24

Grinnan, Daniel, Grant Farr, Adam Fox, and Lori Sweeney. "The Role of Hyperglycemia and Insulin Resistance in the Development and Progression of Pulmonary Arterial Hypertension." Journal of Diabetes Research 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/2481659.

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Pulmonary hypertension is a progressive disorder which often leads to right ventricular failure and death. While the existing classification system for pulmonary hypertension does not account for the impact of diabetes mellitus, evidence is emerging that suggests that diabetes is associated with pulmonary hypertension and that diabetes modifies the course of pulmonary hypertension. There is also growing radiographic, hemodynamic, biochemical, and pathologic data supporting an association between diabetes and pulmonary hypertension. More robust epidemiologic studies are needed to confirm an association between diabetes and pulmonary hypertension and to show that diabetes is a disease modifier in pulmonary hypertension. In addition, evaluating the effects of glucose control in animals with pulmonary hypertension and diabetes (as well as in humans) is warranted.

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25

Saad, M. F., W. C. Knowler, D. J. Pettitt, R. G. Nelson, D. M. Mott, and P. H. Bennett. "Insulin and hypertension. Relationship to obesity and glucose intolerance in Pima Indians." Diabetes 39, no. 11 (November 1, 1990): 1430–35. http://dx.doi.org/10.2337/diabetes.39.11.1430.

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26

Brands, Michael W., and M. Marlina Manhiani. "Sodium-retaining effect of insulin in diabetes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 11 (December 1, 2012): R1101—R1109. http://dx.doi.org/10.1152/ajpregu.00390.2012.

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Insulin has long been hypothesized to cause sodium retention, potentially of enough magnitude to contribute to hypertension in obesity, metabolic syndrome, and Type II diabetes. There is an abundance of supportive evidence from correlational analyses in humans, acute insulin infusion studies in humans and animals, and chronic insulin infusion studies in rats. However, the absence of hypertension in human insulinoma patients, and negative results for sodium-retaining or blood pressure effects of chronic insulin infusion in a whole series of dog studies, strongly refute the insulin hypothesis. We recently questioned whether the euglycemic, hyperinsulinemia model used for most insulin infusion studies, including the previous chronic dog studies, was the most appropriate model to test the renal actions of insulin in obesity, metabolic syndrome, and Type II diabetes. In those circumstances, hyperinsulinemia coexists with hyperglycemia. Therefore, we tested the sodium-retaining effect of insulin in chronically instrumented, alloxan-treated diabetic dogs. We used 24 h/day intravenous insulin infusion to regulate plasma insulin concentration. Induction of diabetes (∼400 mg/dl) caused sustained natriuresis and diuresis. However, if we clamped insulin at baseline, control levels, i.e., prevented it from decreasing, then the sustained natriuresis and diuresis were completely reversed, despite the same level of hyperglycemia. We also found that 24 h/day intrarenal insulin infusion had the same effect in diabetic dogs but had no sodium-retaining action in normal dogs. This new evidence that insulin has a sodium-retaining effect during hyperglycemia may have implications for maintaining sodium balance in uncontrolled Type II diabetes.

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27

Mohan, Gurinder, Ranjeet Kaur, Gursimran Singh Nayyar, and Parminder Singh. "To study the prevalence of insulin resistance in non-diabetes hypertensive subjects." International Journal of Advances in Medicine 4, no. 1 (January 23, 2017): 92. http://dx.doi.org/10.18203/2349-3933.ijam20170035.

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Background: Hypertension is an important medical and public health problem in both developed and developing countries. It is an important risk factor for morbidity and mortality from coronary heart disease, stroke and renal disease. It is well recognized that hypertension coexists in varying degrees with conditions of obesity, insulin resistance/hyperinsulinemia and dyslipidemia, the interrelated metabolic disorders characteristic of metabolic syndrome.Methods: The study was carried out at Sri Guru Ram Das hospital, Amritsar, Punjab, India. A total of 150 patients were taken, out of which 75 were hypertensive and 75 healthy subjects more than 18 years of age were recruited. Serum insulin concentration was measured using a solid phase enzyme linked immunoassay based on the sandwich principle. Insulin resistance was determined by HOMA-IR (homeostasis model assessment of insulin resistance).Results: Statistically, the mean fasting serum insulin level was 17.09±8.17 μIu/ml in cases and 9.33±2.67μIU/ml in controls (reference range 2-25 μIU/ml); the difference was statistically significant (P <0.001). The mean value of HOMA-IR in cases was 3.86±1.84 as compared with controls with mean HOMA -IR value of 2.01±0.62. This difference was statistically significant (P <0.001).Conclusions: Essential hypertension is significantly associated with higher mean fasting insulin levels and insulin resistance. Hyperinsulinemia has a possible role in the pathophysiology of essential hypertension with insulin resistance being the likely predominant mechanism.

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28

Landsberg, Lewis. "HYPERTENSION AND INSULIN RESISTANCE SYNDROME." Endocrine Practice 9, Supplement 2 (October 2003): 63–66. http://dx.doi.org/10.4158/ep.9.s2.63.

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29

Chen, S., C. Yuan, J. F. Schooley, F. J. Haddy, and M. B. Pamnani. "A Consistent Model of Insulin-Dependent Diabetes Mellitus Hypertension." American Journal of Hypertension 5, no. 10 (October 1992): 671–80. http://dx.doi.org/10.1093/ajh/5.10.671.

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30

Hachmi, L. Ben Salem, R. Bouguerra, O. Maatki, H. Smadhi, Z. Turki, S. Hraoui, and C. Ben Slama. "Blood hypertension and insulin therapy in type 2 diabetes." Journal of Hypertension 25, no. 12 (December 2007): A10. http://dx.doi.org/10.1097/01.hjh.0000298993.17516.56.

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31

Trevisan, M., O. Vaccaro, M. Laurenzi, F. De Chiara, M. Di Muro, R. Iacone, and A. Franzese. "Hypertension, non-insulin-dependent diabetes, and intracellular sodium metabolism." Hypertension 11, no. 3 (March 1988): 264–68. http://dx.doi.org/10.1161/01.hyp.11.3.264.

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32

CAZZO, Everton, Martinho Antonio GESTIC, Murillo Pimentel UTRINI, Ricardo Rossetto MACHADO, José Carlos PAREJA, and Elinton Adami CHAIM. "CONTROL OF HYPERTENSION AFTER ROUX-EN-Y GASTRIC BYPASS AMONG OBESE DIABETIC PATIENTS." Arquivos de Gastroenterologia 51, no. 1 (March 2014): 21–24. http://dx.doi.org/10.1590/s0004-28032014000100005.

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Context Hypertension is a common disorder in general practice and has a widely known association with type 2 diabetes mellitus. Low adhesion to clinical treatment may lead to poor results. Obesity surgery can bring early and relevant resolution rates of both morbidities. Objective To describe hypertension evolution after Roux-en-Y gastric bypass in patients with type 2 diabetes mellitus. Method Descriptive observational study designed as a historical cohort of 90 subjects with hypertension and diabetes who underwent Roux-en-Y gastric bypass and were evaluated before and after surgery. Results It was observed a hypertension resolution rate of 85.6% along with markedly decrease in anti-hypertensive usage. Mean resolution time was 3.2 months. Resolution was associated with homeostasis model assessment – insulin resistance, preoperative fasting insulin, anti-hypertensive usage, hypertension time, body mass index and percentage of weight loss. Resolution of hypertension was not statistically associated with diabetes remission within this sample. Conclusion Roux-en-Y gastric bypass was a safe and effective therapeutic tool to achieve hypertension resolution in patients who also had diabetes mellitus.

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33

Passa, Philippe. "Hyperinsulinemia, Insulin Resistance and Essential Hypertension." Hormone Research 38, no. 1-2 (1992): 33–38. http://dx.doi.org/10.1159/000182478.

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34

KHURSHID, MUHAMMAD USMAN, and MANSOOR-UL-HASSAN ALV I. "INSULIN DEPENDENT DIABETES MELLITUS." Professional Medical Journal 16, no. 02 (June 10, 2009): 178–86. http://dx.doi.org/10.29309/tpmj/2009.16.02.2892.

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A i m s & O b j e c t i v e s : To test the hypothesis that an increased plasma concentration of sialic acid, a marker of the acutephaseresponse, is related to the presence of diabetic retinopathy in type 1 diabetes mellitus or Insulin Dependant Diabetes Mellitus (IDDM).R e s e a r c h D e s i g n a n d M e t h o d s : We investigated the relationship between plasma sialic acid concentration and diabetic retinopathy in across-sectional survey of 1,369 people with type 1 diabetes. Subjects were participants in the IDDM Complications Study, which involveddiabetic centers of four different hospitals in Lahore. Results: There was a significantly increasing trend of plasma sialic acid with severityof retinopathy (P < 0.001 in men) and with degree of urinary albumin excretion (P < 0.001 men, P < 0.01 women). Elevated plasma sialicacid concentrations were also associated with several risk factors for diabetic vascular disease: diabetes duration, HbAlc, plasma triglycerideand cholesterol concentrations, waist-to-hip ratio, hypertension and smoking (in men), and low physical exercise (in women). In multiplelogistic regression analysis, plasma sialic acid was independently related to proliferative retinopathy and urinary albumin excretion rate inmen. Conclusions: We concluded that an elevated plasma sialic concentration is strongly related to the presence of microvascularcomplications in type 1 diabetes with retinopathy and nephropathy. Further study of acute-phase response markers and mediators asindicators or predictors of diabetic microvascular complications is therefore justified.

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35

Barreto, Maria Nelly Sobreira de Carvalho, Eduarda Ângela Pessoa Cesse, Rodrigo Fonseca Lima, Michelly Geórgia da Silva Marinho, Yuri da Silva Specht, Eduardo Maia Freese de Carvalho, and Annick Fontbonne. "Analysis of access to hypertensive and diabetic drugs in the Family Health Strategy, State of Pernambuco, Brazil." Revista Brasileira de Epidemiologia 18, no. 2 (June 2015): 413–24. http://dx.doi.org/10.1590/1980-5497201500020010.

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OBJECTIVE: To evaluate the access to drugs for hypertension and diabetes and the direct cost of buying them among users of the Family Health Strategy (FHS) in the state of Pernambuco, Brazil. METHODS: Population-based, cross-sectional study of a systematic random sample of 785 patients with hypertension and 823 patients with diabetes mellitus who were registered in 208 randomly selected FHS teams in 35 municipalities of the state of Pernambuco. The selected municipalities were classified into three levels with probability proportional to municipality size (LS, large-sized; MS, medium-sized; SS, small-sized). To verify differences between the cities, we used the χ2 test. RESULTS: Pharmacological treatment was used by 91.2% patients with hypertension whereas 85.6% patients with diabetes mellitus used oral antidiabetic drugs (OADs), and 15.4% used insulin. The FHS team itself provided antihypertensive medications to 69.0% patients with hypertension, OADs to 75.0% patients with diabetes mellitus, and insulin treatment to 65.4%. The 36.9% patients with hypertension and 29.8% with diabetes mellitus that had to buy all or part of their medications reported median monthly cost of R$ 18.30, R$ 14.00, and R$ 27.61 for antihypertensive drugs, OADs, and insulin, respectively. CONCLUSION: It is necessary to increase efforts to ensure access to these drugs in the primary health care network.

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36

Sharma, A. M., and V. T. Chetty. "Obesity, hypertension and insulin resistance." Acta Diabetologica 42, S1 (April 2005): s3—s8. http://dx.doi.org/10.1007/s00592-005-0175-1.

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37

Bloomgarden, Z. T. "Obesity, Hypertension, and Insulin Resistance." Diabetes Care 25, no. 11 (November 1, 2002): 2088–97. http://dx.doi.org/10.2337/diacare.25.11.2088.

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38

Ferri, C., C. Bellini, G. Desideri, M. Valenti, G. De Mattia, A. Santucci, N. K. Hollenberg, and G. H. Williams. "Relationship between insulin resistance and nonmodulating hypertension: linkage of metabolic abnormalities and cardiovascular risk." Diabetes 48, no. 8 (August 1, 1999): 1623–30. http://dx.doi.org/10.2337/diabetes.48.8.1623.

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39

Meeks, Karlijn A. C., Amy R. Bentley, Adebowale A. Adeyemo, and Charles N. Rotimi. "Evolutionary forces in diabetes and hypertension pathogenesis in Africans." Human Molecular Genetics 30, R1 (March 1, 2021): R110—R118. http://dx.doi.org/10.1093/hmg/ddaa238.

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Abstract Rates of type 2 diabetes (T2D) and hypertension are increasing rapidly in urbanizing sub-Saharan Africa (SSA). While lifestyle factors drive the increases in T2D and hypertension prevalence, evidence across populations shows that genetic variation, which is driven by evolutionary forces including a natural selection that shaped the human genome, also plays a role. Here we report the evidence for the effect of selection in African genomes on mechanisms underlying T2D and hypertension, including energy metabolism, adipose tissue biology, insulin action and salt retention. Selection effects found for variants in genes PPARA and TCF7L2 may have enabled Africans to respond to nutritional challenges by altering carbohydrate and lipid metabolism. Likewise, African-ancestry-specific characteristics of adipose tissue biology (low visceral adipose tissue [VAT], high intermuscular adipose tissue and a strong association between VAT and adiponectin) may have been selected for in response to nutritional and infectious disease challenges in the African environment. Evidence for selection effects on insulin action, including insulin resistance and secretion, has been found for several genes including MPHOSPH9, TMEM127, ZRANB3 and MC3R. These effects may have been historically adaptive in critical conditions, such as famine and inflammation. A strong correlation between hypertension susceptibility variants and latitude supports the hypothesis of selection for salt retention mechanisms in warm, humid climates. Nevertheless, adaptive genomics studies in African populations are scarce. More work is needed, particularly genomics studies covering the wide diversity of African populations in SSA and Africans in diaspora, as well as further functional assessment of established risk loci.

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40

Elliott, W. J. "Insulin Therapy, Hyperglycemia, and Hypertension in Type 1 Diabetes Mellitus." Yearbook of Cardiology 2009 (January 2009): 111–13. http://dx.doi.org/10.1016/s0145-4145(08)79404-8.

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41

Frontoni, Simona, Daniela Bracaglia, and Fabrizio Gigli. "Relationship between autonomic dysfunction, insulin resistance and hypertension, in diabetes." Nutrition, Metabolism and Cardiovascular Diseases 15, no. 6 (December 2005): 441–49. http://dx.doi.org/10.1016/j.numecd.2005.06.010.

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42

Perry, I. J., G. Wannamethee, M. Walker, A. G. Thompson, P. H. Whincup, and A. G. Shaper. "Hypertension and non-insulin-dependent diabetes mellitus: a prospective study." Journal of Hypertension 11, no. 10 (October 1993): 1153–54. http://dx.doi.org/10.1097/00004872-199310000-00043.

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43

Madacsy, L., A. Yasar, T. Tulassay, A. Körner, J. Kelemen, M. Hóbor, and M. Miltényi. "Relative nocturnal hypertension in children with insulin-dependent diabetes mellitus." Acta Paediatrica 83, no. 4 (April 1994): 414–17. http://dx.doi.org/10.1111/j.1651-2227.1994.tb18132.x.

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Doria, Alessandro, Tomio Onuma, Gary Gearin, M. Beatriz S. Freire, James H. Warram, and Andrzej S. Krolewski. "Angiotensinogen Polymorphism M235T, Hypertension, and Nephropathy in Insulin-Dependent Diabetes." Hypertension 27, no. 5 (May 1996): 1134–39. http://dx.doi.org/10.1161/01.hyp.27.5.1134.

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45

de Boer, Ian H. "Insulin Therapy, Hyperglycemia, and Hypertension in Type 1 Diabetes Mellitus." Archives of Internal Medicine 168, no. 17 (September 22, 2008): 1867. http://dx.doi.org/10.1001/archinternmed.2008.2.

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46

Ismail, Nuhad, Bryan Becker, Piotr Strzelczyk, and Eberhard Ritz. "Renal disease and hypertension in non–insulin-dependent diabetes mellitus." Kidney International 55, no. 1 (January 1999): 1–28. http://dx.doi.org/10.1046/j.1523-1755.1999.00232.x.

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47

Yakhontov, D., E. Khilchenko, and D. Tsyrendarzhiev. "CYTOKINE ACTIVITY IN HYPERTENSION ASSOCIATED WITH INSULIN INDEPENDENT DIABETES MELLITUS." Journal of Hypertension 22, Suppl. 2 (June 2004): S369. http://dx.doi.org/10.1097/00004872-200406002-01294.

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48

Feher, M. D. "Hypertension in non-insulin dependent diabetes mellitus and its management." Postgraduate Medical Journal 67, no. 792 (October 1, 1991): 938–46. http://dx.doi.org/10.1136/pgmj.67.792.938.

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Madácsy, L., A. Yasar, T. Tulassay, A. Körner, J. Kelemen, M. Hóbor, and M. Miltényi. "Relative nocturnal hypertension in children with insulin-dependent diabetes mellitus." Pediatric Nephrology 9, no. 3 (June 1995): 391. http://dx.doi.org/10.1007/bf02254225.

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50

Viberti, G. C. "Prevalence of hypertension in Type 1 (insulin-dependent) diabetes mellitus." Diabetologia 34, no. 1 (January 1991): 63–64. http://dx.doi.org/10.1007/bf00404033.

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Journal articles on the topic 'Insulin; Diabetes; Hypertension'

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