scholarly journals Effects of Basal Insulin Analog and Metformin on Glycaemia Control and Weight as Risk Factors for Endothelial Dysfunction

2008 ◽  
Vol 8 (4) ◽  
pp. 309-312 ◽  
Author(s):  
Belma Aščić – Buturović ◽  
Mirsad Kacila

Obese patients with type 2 diabetes and impaired glucose tolerance are at increased risk of development of cardiovascular diseases. Endothelial dysfunction may be a reason for development of atherosclerosis and cardiovascular diseases. Lifestyle modification, increased physical activity, weight reduction, energy restricted diet and good glycaemia control can be useful for the endothelial function improvement and may decrease the risk of cardiovascular diseases. The aim of this study was to evaluate the effects of basal insulin analog and metformin on glycaemia control and weight as risk factors of endothelial dysfunction. Total of 15 patients (9 male and 6 female) with type 2 diabetes were studied. The patients were monitored over six months period. Glycated hemoglobin (HbA1c), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), and body mass index (BMI) were observed. Mean age of the subjects was 53,4 ± 6,27 years. Mean diabetes duration was 3,71 ± 1,89 years. At the end of the study mean body mass index decreased from 27,5 ± 1,45 kg/m2 to 25,7 ±1,22 kg/m2. In this study we included diabetic patients with fasting glycaemia over 7 mmol/ dm3, postmeal glycaemia over 7,8 mmol/dm3 and glycated hemoglobin over 7%. Prior to the study, the patients were treated with premix insulin divided in two daily doses and metformin after the lunch, which did not result in sufficient regulation of glycaemia. We started treatment with one daily insulin basal analog and three daily doses of metformin and monitored the above mentioned parameters. We advised patients to change their lifestyle, to practice energy restricted diet and to increase their daily physical activity. Insulin doses were titrated separately for each patient (0,7-1 IU/kg). Weight reduction was recorded after the study. Mean fasting glycaemia decreased from 8,6±0,49 mmol/dm3 to 7,04±0,19 mmol/dm3 (p < 0,05). Mean postmeal glycaemia decreased from 9,74 ± 0,79 mmol/dm3 to 7,6 ± 0,43 mmol/dm3 (p<0,05). Mean HbA1c decreased from 8,80 ± 0,59 % to 7,11 ± 0,22 % (p<0,05).Treatment with one daily doses of basal insulin analog and three daily doses of metformin with lifestyle modification and weight reduction, in obese patients with type 2 diabetes can be useful for the endothelial function improvement and may decrease the risk of cardiovascular diseases.

2014 ◽  
Vol 6 (2) ◽  
pp. 219-226 ◽  
Author(s):  
Ji‐Hyun Kim ◽  
Ji‐Hyun Ahn ◽  
Soo‐Kyung Kim ◽  
Dae‐Ho Lee ◽  
Hye‐Soon Kim ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Rosa Breton-Romero ◽  
Bihua Feng ◽  
Monika Holbrook ◽  
Melissa G Farb ◽  
Jessica L Fetterman ◽  
...  

Introduction: Diabetes mellitus type 2 is an increasingly public health problem and it is a major cause in the development of cardiovascular diseases. Endothelial dysfunction is a key mechanism that contributes to the pathogenesis of cardiovascular diseases and is a well-known feature of clinical diabetes. Prior studies have demonstrated an impaired nitric oxide bioavailability and a reduced endothelium-dependent vasodilation under diabetic conditions and in animal models, JNK activity has been widely described to be involved in systemic insulin resistance. Hypothesis: Our study aimed to evaluate the involvement of JNK in endothelial dysfunction, studying its potential role in altered eNOS activation and NO synthesis in diabetic patients. Methods: We measured endothelial function and JNK activity in freshly isolated endothelial cells from diabetic patients (n=38) and nondiabetic controls (n=40). Results: ECs from diabetic patients displayed impaired eNOS activation and reduced NO release after insulin and A23187 stimulation, consistent with the presence of endothelial dysfunction. JNK activation was higher in diabetic (**P=0.003), and was associated with lower flow-mediated dilation (r=-0.53, *P=0.02). In endothelial cells from diabetic patients, treatment with JNK chemical inhibitor (SP600125) restored eNOS activation and insulin response (***P<0.001). Nitric oxide bioactivity after A23187 stimuli with diabetes was also recovered in endothelial cells from patients with diabetes. Conclusions: In summary, our data suggest that JNK activation contributes to vascular insulin resistance and endothelial dysfunction in patients with type 2 diabetes and may represent a target in novel therapeutic opportunities.


2005 ◽  
Vol 39 (3) ◽  
pp. 502-507 ◽  
Author(s):  
Jennifer D Goldman-Levine ◽  
Karen W Lee

OBJECTIVE: To review the pharmacology, pharmacokinetics, clinical trial data, adverse effects, and role in therapy of insulin detemir. DATA SOURCES: Articles and meeting abstracts were identified through searches of MEDLINE (1996–June 2004), EMBASE (1980–June 2004), and International Pharmaceutical Abstracts (1970–June 2004) databases, and unpublished information was provided by the manufacturer. STUDY SELECTION AND DATA EXTRACTION: All available studies relating to insulin detemir's pharmacology were selected. Only human studies were used for pharmacokinetic, drug interaction, efficacy, and safety data. DATA SYNTHESIS: Insulin detemir is a basal insulin analog that has been shown to improve glycemic control in patients with type 1 and type 2 diabetes. CONCLUSIONS: Insulin detemir offers some benefits over NPH for use as basal insulin in patients with type 1 and type 2 diabetes.


2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Alaaeldin Bashier ◽  
Azza Bin Hussain ◽  
Elamin Abdelgadir ◽  
Fatheya Alawadi ◽  
Hani Sabbour ◽  
...  

Abstract The recent American Diabetes Association and the European Association for the Study of Diabetes guideline mentioned glycaemia management in type 2 diabetes mellitus (T2DM) patients with cardiovascular diseases (CVDs); however, it did not cover the treatment approaches for patients with T2DM having a high risk of CVD, and treatment and screening approaches for CVDs in patients with concomitant T2DM. This consensus guideline undertakes the data obtained from all the cardiovascular outcome trials (CVOTs) to propose approaches for the T2DM management in presence of CV comorbidities. For patients at high risk of CVD, metformin is the drug of choice to manage the T2DM to achieve a patient specific HbA1c target. In case of established CVD, a combination of glucagon-like peptide-1 receptor agonist with proven CV benefits is recommended along with metformin, while for chronic kidney disease or heart failure, a sodium–glucose transporter proteins-2 inhibitor with proven benefit is advised. This document also summarises various screening and investigational approaches for the major CV events with their accuracy and specificity along with the treatment guidance to assist the healthcare professionals in selecting the best management strategies for every individual. Since lifestyle modification and management plays an important role in maintaining the effectiveness of the pharmacological therapies, authors of this consensus recommendation have also briefed on the patient-centric non-pharmacological management of T2DM and CVD.


Author(s):  
Y. Durgarao ◽  
Poornima A. Manjrekar ◽  
Prabha Adhikari ◽  
M. Chakrapani ◽  
M.S. Rukmini

Vitamin D, a steroid hormone is primarily known for its role in calcium and bone mineral homeostasis. Over the years, vitamin D has been implicated in various non-skeletal diseases. The extraskeletal phenomenon can be attributed to the presence of vitamin D receptors (VDRs) in almost all cells and identification of 1-α hydroxylase in extrarenal tissues. The vitamin D deficiency (VDD) pandemic was globally reported with increasing evidence and paralleled the prevalence of diabetes, obesity and cardiovascular diseases (CVDs). A dependent link was proposed between hypovitaminosis D glycemic status, insulin resistance and also the other major factors associated with type 2 diabetes leading to CVDs. Insulin resistance plays a central role in both type 2 diabetes and insulin resistance syndrome. These 2 disorders are associated with distinct etiologies including hypertension, atherogenic dyslipidemia, and significant vascular abnormalities that could lead to endothelial dysfunction. Evidence from randomised clinical trials and meta-analysis, however, yielded conflicting results. This review summarizes the role of vitamin D in the regulation of glucose homeostasis with an emphasis on insulin resistance, blood pressure, dyslipidaemia, endothelial dysfunction and related cardiovascular diseases and also underline the plausible mechanisms for all the documented effects.


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