scholarly journals New Blood Pressure Targets In Non-Diabetic Patients And Insulin Resistance In Brain

2016 ◽  
Vol 12 (1) ◽  
pp. 111-112
Author(s):  
S Galoi
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Diabetic Patients ◽  
Blood Pressure Targets

Shedding of TNF-α receptors, blood pressure, and insulin sensitivity in type 2 diabetes mellitus

2002 ◽  
Vol 282 (4) ◽  
pp. E952-E959 ◽  
Author(s):  
José-Manuel Fernandez-Real ◽  
Begoña Lainez ◽  
Joan Vendrell ◽  
Mercedes Rigla ◽  
Antoni Castro ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Diabetic Patients ◽  
Blood Monocytes ◽  
Tnf Α ◽  
Exercise Induced ◽  
Factor Α ◽  
Genetically Determined

Tumor necrosis factor-α (TNF-α) is increasingly recognized as a key component in the development of insulin resistance and increased blood pressure. In a sample of 368 individuals, the ratio of soluble TNF-α receptors (sTNFR2/sTNFR1) correlated positively with systolic and diastolic blood pressure ( P < 0.01). This ratio was significantly greater in type 2 diabetic subjects (DM-2) than in type 1 diabetic patients and was greater than in control nondiabetic subjects ( P < 0.00001). The TNF-α receptor 1 (TNFR1) density in peripheral blood monocytes was similar in DM-2 patients and in nondiabetic subjects. After phorbol 12-myristate 13-acetate, TNFR1 shedding was significantly decreased in DM-2 compared with control subjects, and it was directly associated with insulin sensitivity ( r = 0.54, P = 0.03). Serum sTNFR1 concentration was also linked to the vasodilatory response to glyceryltrinitrate ( P = 0.01). Conversely, TNF-α receptor 2 shedding was negatively associated with insulin sensitivity ( r = −0.54, P = 0.03), whereas shedding of L-selectin showed no significant association. After exercise-induced lowering of blood pressure, a parallel decrease in sTNFR2/sTNFR1 was observed in DM-2 patients. Our findings suggest that insulin resistance and blood pressure are linked to altered shedding of TNF-α receptors in DM-2. The latter seems reversible and is not genetically determined.

scholarly journals Effect of sodium intake on blood pressure and albuminuria in Type 2 diabetic patients: the role of insulin resistance

Diabetologia ◽  
2003 ◽  
Vol 47 (2) ◽  
pp. 300-303 ◽  
Author(s):  
M. Vedovato ◽  
G. Lepore ◽  
A. Coracina ◽  
A. R. Dodesini ◽  
E. Jori ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Sodium Intake ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

scholarly journals Hypertension in Diabetes: An Update of Basic Mechanisms and Clinical Disease

Hypertension ◽  
2021 ◽  
Author(s):  
Guanghong Jia ◽  
James R. Sowers
Keyword(s):  
Insulin Resistance ◽  
Molecular Mechanisms ◽  
Treatment Strategies ◽  
Epidemiological Studies ◽  
Diabetic Patients ◽  
Epithelial Sodium Channels ◽  
Mitochondria Dysfunction ◽  
Blood Pressure Targets ◽  
Sodium Glucose Cotransporter ◽  
Underlying Mechanisms

Epidemiological studies have documented that insulin resistance and diabetes not only constitute metabolic abnormalities but also predispose to hypertension, vascular stiffness, and associated cardiovascular disease. Meanwhile, excessive arterial stiffness and impaired vasorelaxation, in turn, contribute to worsening insulin resistance and the development of diabetes. Molecular mechanisms promoting hypertension in diabetes include inappropriate activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, mitochondria dysfunction, excessive oxidative stress, and systemic inflammation. This review highlights recent studies which have uncovered new underlying mechanisms for the increased propensity for the development of hypertension in association with diabetes. These include enhanced activation of epithelial sodium channels, alterations in extracellular vesicles and their microRNAs, abnormal gut microbiota, and increased renal sodium-glucose cotransporter activity, which collectively predispose to hypertension in association with diabetes. This review also covers socioeconomic factors and currently recommended blood pressure targets and related treatment strategies in diabetic patients with hypertension.

scholarly journals Characteristics of diabetic patients associated with achieving and maintaining blood pressure targets in the Adherence and Intensification of Medications program

2013 ◽  
Vol 10 (1) ◽  
pp. 60-73 ◽  
Author(s):  
Mandi L Klamerus ◽  
Eve A Kerr ◽  
Hayden B Bosworth ◽  
Julie A Schmittdiel ◽  
Michele Heisler
Keyword(s):  
Blood Pressure ◽  
Diabetic Patients ◽  
Blood Pressure Targets

scholarly journals A breakthrough-like effect of metformin reduces peripheral resistance to triiodothyronine in euthyroid, non-insulin-resistant, type 2 diabetic patients

2021 ◽  
Author(s):  
Melinda Kertész ◽  
Szilárd Kun ◽  
Eszter Sélley ◽  
Zsuzsanna Nagy ◽  
Tamás Kőszegi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
In Vitro Study ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Akt Phosphorylation ◽  
Type 2 Diabetic

Background: Type 2 diabetes is characterized, beyond the insulin resistance, by polyhormonal resistance. Thyroid hormonal resistance has not yet been described in this population of patients. Metformin is used to decrease insulin resistance, and at present it is assumed to influence the effect of triiodothyronine, as well. Methods: In this open label, pilot, hypothesis generating, follow-up study 21 patients were included, all of them euthyroid with drug naïve, newly diagnosed type 2 diabetes. Before and after four weeks of metformin therapy fructosamine, homeostasis model assessment for insulin resistance (HOMA-IR), thyroid hormones, T3/T4 ratio, and TSH, as well as blood pressure and heart rate using ambulatory blood pressure monitor were measured. We also conducted an in vitro study to investigate the possible mechanisms of T3 resistance, assessing T3 induced Akt phosphorylation among normal (5 mM) and high (25 mM) glucose levels with or without metformin treatment in a human embryonal kidney cell line. Results: Metformin decreased the level of T3 (p<0.001), the ratio of T3/T4 (p=0.038), fructosamine (p=0.008) and HOMA-IR (p=0.022). All these changes were accompanied by an unchanged TSH, T4, triglyceride, plasma glucose, bodyweight, blood pressure and heart rate. In our in vitro study, T3 induced Akt phosphorylation decreased in cells grown in 25 mM glucose medium compared to those in 5 mM. Metformin could not reverse this effect. Conclusion: Metformin seems to improve T3 sensitivity in the cardiovascular system in euthyroid, type 2 diabetic patients, the mechanism of which may be supracellular.

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