Metformin attenuates progression of carotid arterial wall thickness in patients with type 2 diabetes

Matsumoto, Kazunari; Sera, Yoshihisa; Abe, Yasuyo; Tominaga, Tan; Yeki, Yukitaka; Miyake, Seibei

doi:10.1016/j.diabres.2003.11.007

Cited by 73 publications

(57 citation statements)

References 10 publications

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“…Recently published results from the Hyperinsulinaemia: the Outcome of its Metabolic Effects (HOME) trial have shown that metformin improves macrovascular outcomes in insulin-treated type 2 diabetes patients [71]. This is consistent with some data, including from one of the present authors (J. R. Petrie), that metformin may have intrinsic (and possibly direct) beneficial effects independent of glucose lowering on the cardiovascular system via activation of AMPK [72][73][74] in a number of conditions [72,75,76]. If this is accepted, the hypothesis that metformin might prevent cardiovascular complications in type 1 diabetes should also be tested formally, as even young adults with this condition have an extremely high relative risk of CVD [77][78][79].…”

Section: Studysupporting

confidence: 79%

The use of metformin in type 1 diabetes: a systematic review of efficacy

et al. 2010

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Aims/hypothesis As adding metformin to insulin therapy has been advocated in type 1 diabetes, we conducted a systematic review of published clinical trials and clinical trial databases to assess the effects on HbA 1c , weight, insulin-dose requirement and adverse effects. Methods We constructed evidence tables and fitted a fixedeffects model (inverse variance method) in order to assess heterogeneity between studies and give a crude measure of each overall treatment effect. Results Of 197 studies identified, nine involved randomisation with informed consent of patients with type 1 diabetes to metformin (vs placebo or comparator) in either a parallel or crossover design for at least 1 week. We noted marked heterogeneity in study design, drug dose, age of participants and length of follow-up. Metformin was associated with reductions in: (1) insulin-dose requirement (5.7-10

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Section: Studysupporting

confidence: 79%

The use of metformin in type 1 diabetes: a systematic review of efficacy

et al. 2010

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“…The annual increase rate of IMT adjusted for other clinical factors was significantly smaller in A group than in D group, and it was actually a negative value in A group, meaning that regression of IMT from the baseline was achieved by near normalization of HbA1c level for three years. Pioglitazone, metformin and a-glucosidase inhibitor, voglibose, were previously reported to reduce the IMT increase independently of glycemic control in type 2 diabetic patients [11][12][13]. While these oral agents having extra-pancreatic actions did not differ between the two groups, the proportion of the patients with insulin secretagogue (sulfonylurea or nateglinide) was significantly lower in A group than in D group (12% vs. 43%, c 2 = 9.71, p = 0.002) as shown in Table 3.…”

Section: Discussionmentioning

confidence: 99%

Strict Glycemic Control Ameliorates the Increase of Carotid IMT in Patients with Type 2 Diabetes

et al. 2006

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Abstract. The aim of this study was to investigate the effect of strict glycemic control on the carotid artery intima-media thickness (IMT) in type 2 diabetic patients who initially had good glycemic control (HbA1c between 5.8 and 6.4 %). The subjects were 67 patients showing deterioration of the mean HbA1c over 3 years by more than 0.2% from baseline (D group) and 33 subjects showing improvement of the mean HbA1c by more than 0.2% from baseline (A group). The clinical characteristics and annual change of IMT during the observation period were compared between the two groups in a 3-year retrospective longitudinal study. The baseline characteristics and the mean values of BMI, blood pressure, and serum lipids during the study period did not differ significantly between the two groups. However, the mean HbA1c of A group was significantly lower than that of D group (5.67 ± 0.10 vs. 6.28 ± 0.08, mean ± SE, p<0.001). The adjusted annual increase rate of IMT was significantly less in A group than in D group (-0.035 ± 0.019 vs. 0.036 ± 0.015 mm, M ± SEM, p<0.001). These results indicate that further improvement of glycemic control from a good HbA1c value can prevent an increase of IMT in type 2 diabetic patients. IT is well-known that the onset and progression of atherosclerosis is much more rapid in diabetic patients than healthy non-diabetic subjects, and one of the major causes of death in diabetes is atherosclerotic diseases. Thus, strict glycemic control is important to prevent the onset and progression of atherosclerosis. The UK Prospective Diabetes Study (UKPDS), a largescale prospective study of newly diagnosed type 2 diabetic patients, showed that every 1% decrease of HbA1c could reduce the incidence of myocardial infarction and stroke by 14% and 11%, respectively [1]. However, the UKPDS failed to show a significant reduction in the incidence of stroke and myocardial infarction in the intensive glycemic control group (median HbA1c: 7.0%) compared with the conventional glycemic control group (median HbA1c: 7.9%) over 15 years [2]. These results suggest that much stricter glycemic control and an HbA1c below 7.0% may be needed to prevent atherosclerosis in diabetic patients. The Japan Diabetes Society (JDS) had proposed an HbA1c from 5.8% to 6.4% as a marker of good control, with less than 5.7% as excellent control. However, there is no evidence as to whether the risk of atherosclerosis can be decreased by further reducing HbA1c levels from the good control range (5.8-6.4%) to the excellent range (£5.7%) in Japanese type 2 diabetic patients. Therefore, many diabetic patients with good control are maintained at such HbA1c levels, and no attempts are made to achieve excellent control. We previously reported a method of measuring carotid artery intima-media thickness (IMT) by B-mode ultrasonography and showed that the IMT of subjects with diabetes was larger than that of age-matched subjects with normal glucose tolerance [3,4]. Previous

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“…Esta acción le adiciona otro potencial beneficio a la metformina, la modulación de inflamación en la fibrosis pulmonar idiopática asociada a bleomicina 71 . Al disminuir la expresión de colágeno y fibronectina se reduce el grosor de la pared del vaso, es así como a través de distintos estudios se ha observado la disminución en el grosor de la Íntima Media (IMT) en especial el de la Carótida (cIMT) posterior a un año de tratamiento con metformina 72 . En un estudio prospectivo, se evidenció que la metformina a dosis de 500 a 750 mg/día atenuaba la progresión del IMT carotideo a los dos años de tratamiento 72 ; hallazgos similares fueron descritos en la cohorte de tres años de pacientes diabéticos en donde el cambio anual en cIMT promedio del grupo de glibenclamida y metformina (0,003 +/-0,048 mm) fue menor que la del grupo de glibenclamida (0,064 +/-0,045 mm) y el grupo gliclazida (0,032 +/-0,036 mm) (p <0,0001 y p = 0,043 respectivamente) 73 .…”

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“…Al disminuir la expresión de colágeno y fibronectina se reduce el grosor de la pared del vaso, es así como a través de distintos estudios se ha observado la disminución en el grosor de la Íntima Media (IMT) en especial el de la Carótida (cIMT) posterior a un año de tratamiento con metformina 72 . En un estudio prospectivo, se evidenció que la metformina a dosis de 500 a 750 mg/día atenuaba la progresión del IMT carotideo a los dos años de tratamiento 72 ; hallazgos similares fueron descritos en la cohorte de tres años de pacientes diabéticos en donde el cambio anual en cIMT promedio del grupo de glibenclamida y metformina (0,003 +/-0,048 mm) fue menor que la del grupo de glibenclamida (0,064 +/-0,045 mm) y el grupo gliclazida (0,032 +/-0,036 mm) (p <0,0001 y p = 0,043 respectivamente) 73 . Tales hallazgos, además de ser soportados por la modificación en el colágeno y la fibronectina, también pueden ser explicados debido a la acción de la metformina al inhibir la proliferación de células del músculo liso aórtico, la expresión de metaloproteinasa de matriz 74 tipo-2 y producción de ROS, a través de la inhibición de la NADPH oxidasa y Protein Kinasas C que suprime el efecto de la leptina sobre la producción de ROS.…”

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Metformina: más allá del control glucémico

Morantes-Caballero

Londoño-Zapata

Rubio-Rivera

et al. 2017

revmed

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RESUMENIntroducción: la metformina es una biguanida que disminuye gluconeogénesis e incrementa la recaptación de glucosa en los músculos, sin embargo, más allá del glucémico se han documentado beneficios adicionales como la disminución de complicaciones crónicas derivadas de la hiperglucemia, entre ellas las cardiovasculares y del síndrome metabólico per se. Objetivo: identificar los efectos de la metformina diferentes al control control glucémico en población con diabetes mellitus, con el fin de contribuir a difundir el conocimiento. Materiales y método: tres revisores independientes realizaron la búsqueda en distintas bases de datos entre ellas Pubmed y ScienceDirect, utilizando los términos Metfomin AND Cardiovascular disease AND inflamatory response AND Hyperlipidemia, Biguanides, Diabetes Mellitus, Diabetes complications, Obesity, Vascular diseases AND Cancer; y Metfomina y enfermedad cardiovascular, metformina y cáncer se seleccionaron los artículos desde el año 2010, encontrando 13 828 artículos, de los cuales se incluyeron 144. Conclusión: más allá del control glucémico, la metformina, modifica la "memoria metabólica", reduce mediadores inflamatorios y el grosor de pared arterial, disminuye factores trombóticos y reduce la prevalencia de falla cardiaca logrando impactar la morbimortalidad y mediante cambios moleculares o genéticos, tiene potencial uso como anticancerígeno. El clínico debe conocer estos efectos para favorecer su pronto inicio en los casos indicados. Metformin: beyond the glycemic targetABSTRACT Introduction: the metformin is a biguanide which main action is to decrease hepatic glucose output, primarily by decreasing gluconeogenesis, and increase glucose uptake by muscles. However, beyond the glycemic target, additional benefits have been documented like a decrease in chronic complications to hyperglycemia, including cardiovascular comorbility and metabolic syndrome. Objetive: to identify effects of metformin other than glycemic control in patients with diabetes mellitus in order to help disseminate knowledge. Materials and methods: three independent reviewers searched in different databases of PubMed and ScienceDirect using the DeCS and MeSH terms: Metfomin AND Cardiovascular disease AND inflamatory response AND Hyperlipidemia, Biguanides, Diabetes Mellitus, Diabetes complications,Obesity, Vascular diseases AND Cancer, selecting the items since 2010 year and prior to warrant mention. Search based publications that were considered most relevant and, additionally, a manual search of the referenced articles in publications retrieved in the initial search was conducted, 13 828 articles were found but 144 were included finally. Conclusion: beyond glycemic control, Metformin, modifies the "metabolic memory", reduces inflammatory mediators and thickness of arterial wall, decreases thrombotic factors and reduces the prevalence of heart failure making an impact morbidity and mortality and because of molecular or genetic changes, it has potential use as anticarcinogenic. The physicians should know...

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Metformin attenuates progression of carotid arterial wall thickness in patients with type 2 diabetes

Cited by 73 publications

References 10 publications

The use of metformin in type 1 diabetes: a systematic review of efficacy

The use of metformin in type 1 diabetes: a systematic review of efficacy

Strict Glycemic Control Ameliorates the Increase of Carotid IMT in Patients with Type 2 Diabetes

Metformina: más allá del control glucémico

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