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Relevant bibliographies by topics / Insulin; Diabetes; Hypertension

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Academic literature on the topic 'Insulin; Diabetes; Hypertension'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "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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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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Dissertations / Theses on the topic "Insulin; Diabetes; Hypertension"

1

Al-Hussary, Nabeel A. J. "Insulin receptor binding in hypertension and non-insulin dependent diabetes mellitus." Thesis, Aston University, 1986. http://publications.aston.ac.uk/14510/.

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Pinkney, Jonathan Henley. "Origins of hypertension in non-insulin dependent diabetes." Thesis, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286682.

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3

Wiggam, Malcolm Ivan. "Aspects of insulin resistance in essential hypertension and insulin-dependent diabetes mellitus." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387971.

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4

Petrie, John Ross. "Serum insulin concentrations, insulin sensitivity, and endothelial function in essential hypertension and non-insulin-dependent diabetes mellitus." Thesis, University of Glasgow, 1997. http://theses.gla.ac.uk/2846/.

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A series of studies is described in which specific and conventional insulin immunoassays, the hyperinsulinaemic clamp technique and forearm venous occlusion plethysmography with local intra-arterial infusions have been used to investigate: the effect of insulin assay specificity on the relationships among serum insulin concentrations, insulin sensitivity, and blood pressure in diabetic and non-diabetic subjects with and without essential hypertension (Chapter 5) the effect of sustained physiological activation of the renin-angiotensin system induced by moderate dietary sodium restriction on insulin sensitivity in patients with non-insulin-dependent diabetes mellitus (Chapter 6) the relationship between endothelial function and insulin sensitivity in healthy subjects (Chapter 7) Prior to these investigations, preliminary studies (Chapters 3 and 4) were performed in order to validate aspects of the clinical physiological techniques required for the measurement of blood flow and insulin sensitivity. The reproducibility of bilateral forearm venous occlusion plethysmography Studies using this technique to measure changes in forearm blood flow (FBF) during intra-arterial infusions of vasoactive substances often report changes in blood flow ratio (expressing responses in the intervention arm as a ratio of responses in the control arm) rather than absolute values for flow. However, unilateral measurements are reported by other investigators, and the possibility was considered that the method used for expressing responses might influence the conclusions reached. A reproducibility study was performed (Chapter 3) which demonstrated that the between-day intra-subject variability of bilateral forearm venous occlusion plethysmography (FBF ratios) was less than that of unilateral FBF measurements. The bilateral technique was used thereafter where possible.

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5

Courtney, Hamish. "Determinants of insulin action : physiological and therapeutic implications." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343100.

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6

Fryer, Lee George Daniel. "Studies into the role of glucose transporter function in insulin resistance." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265007.

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7

Sanderson, Alison Louise. "Regulation of skeletal muscle metabolism." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318615.

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8

Hopkinson, Helen Elizabeth. "Betaâ†2-adrenoceptor signalling and the effect of insulin." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301070.

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9

Wong, Siu-hing, and 王少鑫. "Relationship between resistant hypertension and sodium intake in type 2 diabetes Hong Kong Chinese." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46373445.

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10

Marinik, Elaina. "Angiotensin II receptor blockade and insulin sensitivity in overweight and obese adults with elevated blood pressure." Diss., Virginia Tech, 2012. http://hdl.handle.net/10919/37369.

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Currently, it is reported that ~65% and 34% of the U.S. population is overweight and obese, respectively. Obesity is a major risk factor for cardiovascular disease. Overweight and obese individuals are also at an increased risk of developing hypertension. Whole-body insulin sensitivity is reduced in obesity, resulting in insulin resistance and increased risk of type 2 diabetes. One possible mechanism contributing to insulin resistance in obesity hypertension is renin-angiotensin system (RAS) overactivation. The RAS exhibits vasocontricting and sodium-retaining properties, yet in vivo and in vitro animal experiments suggest impairment of whole-body insulin sensitivity with increased angiotensin II (Ang II) exposure. Furthermore, evidence from clinical studies indicates Ang II receptor blockers (ARBs) may reduce the incidence of new-onset diabetes compared to other antihypertensive agents in at-risk hypertensive patients. However, it is unclear if whole-body insulin sensitivity is improved with Ang II receptor blockade in humans. Thus, we tested the hypothesis that 8-week Ang II receptor blockade with olmesartan would improve whole-body insulin sensitivity in overweight and obese individuals with elevated blood pressure (BP). Olmesartan was selected for the present study because it is devoid of partial PPARÎ³ agonist activity. To test our hypothesis, intravenous glucose tolerance tests were performed to measure insulin sensitivity before and after control and ARB treatment in a randomized crossover manner. Because skeletal muscle tissue accounts for ~75-90% of insulin-stimulated glucose uptake, a secondary exploratory aim was to examine skeletal muscle inflammatory and collagen response in relation to insulin sensitivity during ARB treatment. No baseline differences were observed between treatments (P>0.05). Both systolic (-11.7 mmHg; P=0.008) and diastolic (-12.1 mmHg; P=0.000) BP were reduced with ARB treatment. Insulin sensitivity was not different between treatments (P>0.05). No correlates of insulin sensitivity were identified. In addition, skeletal muscle inflammatory and collagen gene expression did not change from pre- to post-ARB treatment (P>0.05). Our findings suggest that short-term RAS blockade in overweight and obese adults with elevated BP does not improve whole-body insulin sensitivity, despite a significant BP reduction. Further studies are needed to clarify the role of individual RAS blockers on insulin sensitivity during RAS inhibition in obesity hypertension.
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Books on the topic "Insulin; Diabetes; Hypertension"

1

Al-Hussary, Nabeel Ahmad Jargees. Insulin receptor binding in hypertension and non-insulin dependent diabetes mellitus. Birmingham: Aston University. Department of Molecular Sciences, 1986.

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2

European Symposium on Metabolism (8th 2002 Padua, Italy). The metabolic syndrome: Diabetes, obesity, hyperlipidemia & hypertension : proceedings of the 8th European Symposium on Metabolism, held in Padua, Italy, between 2 and 5 October 2002. Edited by Crepaldi Gaetano, Tiengo Antonio, and Avogaro Angelo. Amsterdam: Elsevier, 2003.

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3

Association, American Diabetes, ed. American Diabetes Association guide to medical nutrition therapy for diabetes. 2nd ed. Alexandria, Va: American Diabetes Association, 2012.

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4

Berenson, Gerald S. Evolution of Cardio-Metabolic Risk from Birth to Middle Age: The Bogalusa Heart Study. Dordrecht: Springer Science+Business Media B.V., 2011.

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5

Clinical Management of Hypertension in Diabetes. London: Taylor & Francis Group Plc, 2004.

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6

Clinical Management Hypertention Diabetes. Informa Healthcare, 2001.

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7

Levy, David. Macrovascular complications, hypertension, and lipids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0008.

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Premature vascular disease is common in Type 1 diabetes, especially in women and those with long duration. Many studies have identified early vascular involvement, using carotid Doppler and coronary artery calcification. Symptoms of coronary heart disease are often absent or muted, and the best methods for identifying occult coronary heart disease in Type 1 patients are not known. The concept of ideal cardiovascular health is valuable in planning preventive lifestyle and medical interventions. ‘Essential’ hypertension in young Type 1 patients is common, and reflects increased arterial stiffness. Hypertension is invariable in patients with any degree of albuminuria or renal impairment. Statin treatment in patients over 40 years old is recommended, but the evidence base is weak. Statins and ezetimibe are the only agents of prognostic value currently available for prevention of vascular events. Primary prevention with aspirin needs individual assessment. Insulin resistance/metabolic syndrome is frequent in Type 1 diabetes.

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8

Markolf, Hanefeld, and Leonhardt Wolfgang, eds. The metabolic syndrome: An integrated concept for the diagnosis and therapy of a cluster of diseases of civilisation. Jena: G. Fischer, 1997.

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9

(Editor), Gaetano Crepaldi, Antonio Tiengo (Editor), and Angelo Avogaro (Editor), eds. The Metabolic Syndrome: Diabetes, Obesity, Hyperlipidemia and Hypertension: Proceedings of the 8th European Symposium on Metabolism, Padua, Italy, 2-5 October 2002, ICS 1253 (International Congress). Elsevier, 2003.

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10

Design, SilentGnogaArt. Blood Sugar Blood and Pressure Log Book: Daily Health Journal Hypertension and Diabetes Diary BLOOD GLUCOSE INSULIN UNITS BLOOD PRESSURE MEDICINES BODY WEIGHT Size 6x9 Inch. Independently Published, 2020.

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Book chapters on the topic "Insulin; Diabetes; Hypertension"

1

Galipeau, Denise, and John H. Mcneill. "Insulin Resistance and Experimental Hypertension." In Atherosclerosis, Hypertension and Diabetes, 247–60. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9232-1_20.

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2

Natali, Andrea, Stefano Taddei, and Ele Ferrannini. "Hypertension and Insulin Resistance." In Clinical Research in Diabetes and Obesity, 301–22. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-3906-0_16.

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3

Lautt, W. WAYNE. "New Paradigm for Insulin Resistance: the Hiss Story." In Atherosclerosis, Hypertension and Diabetes, 263–76. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9232-1_21.

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4

Gans, Rijk O. B., and A. B. J. M. Donker. "Insulin and Blood Pressure." In The Kidney and Hypertension in Diabetes Mellitus, 261–71. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-6746-9_25.

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Gans, Rijk O. B., and Ab J. M. Donker. "Insulin and Blood Pressure." In The Kidney and Hypertension in Diabetes Mellitus, 289–97. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-6749-0_29.

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6

Schmitz, Ole. "Aspects of Insulin Treatment in Uremic Insulin-Dependent Diabetic Patients before and after Active Replacement Therapy." In The Kidney and Hypertension in Diabetes Mellitus, 379–88. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-1974-1_44.

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7

Verma, Subodh, and John H. McNeill. "Alterations in the Vascular Actions of Insulin in the Pathogenesis of Insulin Resistance and Hypertension." In Diabetes and Cardiovascular Disease, 133–42. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1321-6_18.

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8

Schmitz, Anita. "Microalbuminuria and Mortality in Non-Insulin-Dependent Diabetes." In The Kidney and Hypertension in Diabetes Mellitus, 65–70. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-1974-1_9.

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9

Solini, Anna, and Ralph A. Defronzo. "Hypertension, Cardiovascular Disease, Diabetes Mellitus, and Diabetic Nephropathy: Role of Insulin Resistance." In The Kidney and Hypertension in Diabetes Mellitus, 37–51. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-6746-9_4.

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10

Solini, Anna, and Ralph A. DeFronzo. "Hypertension, Cardiovascular Disease, Diabetes Mellitus, and Diabetic Nephropathy: Role of Insulin Resistance." In The Kidney and Hypertension in Diabetes Mellitus, 61–74. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-6749-0_7.

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Conference papers on the topic "Insulin; Diabetes; Hypertension"

1

Gita, Anggi Putri Aria, Isna Qadrijati, and Bhisma Murti. "Biopsychosocial Determinants of Diabetes Mellitus Type 2: Evidence from Surakarta, Central Java." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.01.46.

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ABSTRACT Background: Stress has been shown to have major effects on metabolic activity. Diabetes mellitus (DM) is a metabolic disease characterized by chronic hyperglycemia that results from an alteration of the secretion or action of insulin. This study aimed to investigate biopsychosocial determinants of diabetes mellitus type 2 Subjects and Method: A case control study was conducted in Surakarta, Centra Java, Indonesia, from November 2019 to January 2020. A sample of 200 patients with type 2 DM was selected by fixed disease sampling. The dependent variable was type 2 DM. The independent variables were family history of DM, dietary pattern, physical activity, body mass index (BMI), central obesity, stress, hypertension, and smoking. The data were collected by medical record and questionnaire. The data were analyzed by a multiple logistic regression run on Stata 13. Results: The risk of type 2 DM increased with family history of tipe 2 DM (OR= 12.88; 95% CI= 5.18 to 32.04; p<0.001), poor dietary pattern (OR= 2.92; 95% CI= 1.16 to 7.36; p= 0.023), and low physical activity (OR= 3.15; 95% CI= 1.22 to 8.18; p= 0.018), central obesity (OR= 4.55; 95% CI= 1.55 to 13.41; p= 0.006), stress (OR= 3.07; 95% CI= 1.21 to 7.79; p= 0.018), history of hypertension (OR= 3.83; 95% CI= 1.49 to 9.79; p= 0.005), and smoking behavior (OR= 3.86; 95% CI= 1.29 to 11.57; p= 0.016). The risk of type 2 DM decreased with normal BMI (OR= 0.37; 95% CI= 0.13 to 1.01; p= 0.053). Conclusion: The risk of type 2 DM increases with family history of tipe 2 DM, poor dietary pattern, and low physical activity, central obesity, stress, history of hypertension, and smoking behavior. The risk of type 2 DM decreases with normal BMI. Keywords: Determinan biopsikososial, DM tipe 2. Correspondence: Anggi Putri Aria Gita. Masters Program in Public Health, Universitas Sebelas Maret, Jl. Ir. Sutami 36A, Surakarta 57126, Central Java, Indonesia. Email: anggipag@gmail.com. Mobile: +628975406464. DOI: https://doi.org/10.26911/the7thicph.01.46

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