Acarbose may indirectly prevent the occurrence of cardiac problems

Acarbose may

Acarbose may

Acarbose may indirectly prevent the occurrence of cardiac problems by controlling metabolic parameters and reducing inflammatory markers.

Noushin Khalili and Alireza Safavipour



Table 1: Acarbose effect on Inflammatory markers before and after Intervention


Metabolic syndrome (MetS) refers to a cluster of risk factors for cardiovascular disease and type 2 diabetes. The aim of this study is to assess the effects of acarbose as an antihyperglycemic agent (drug) on late complications of MetS.

Table 2: Effect on Body weight and Waist circumference

Data shown mean±SD; CRP: C-reactive protein; FMD: Flow-mediated dilation; IMT: Intima-media thickness; EFT: Epicardial fat thickness; MetS: Metabolic syndrome; WC: Waist circumference; CVDs: Cardiovascular diseases; CV: Cardiovascular


This double-blind randomized clinical trial was done on patients with MetS admitted to Isfahan Endocrine and Metabolism Research Center. They were assigned randomly to two groups: A who received acarbose (n = 32) and group B who received a placebo (n = 42) for 6 months. Cardiovascular indexes including flow-mediated dilation (FMD), intima-media thickness (IMT), epicardial fat thickness (EFT), and C-reactive protein (CRP) were measured at baseline and 6 months after the treatment and compared between the two groups.


Post-intervention mean of weight (mean difference: −2.5 ± 0.89) and abdominal obesity (mean difference: −2.2 ± 0.64) in acarbose group were significantly decreased (P value < 0.001). High-density lipoprotein (HDL) level in acarbose group was significantly higher than control group (44.7 ± 7.6 vs 41.1 ± 6.4; P value = 0.043), while the other metabolic parameters were not significantly different between the two groups (P value > 0.05). In both groups, CRP and EFT decreased significantly after the intervention, and the levels of CRP, EFT, and IMT markers in the acarbose group were significantly lower than control group (P value < 0.05).


The administration of acarbose in patients with MetS can decrease weight and abdominal obesity as well as the reduction of inflammatory and cardiovascular markers, including CRP, EFT, and IMT and also increases HDL.

Keywords: AcarbosecardiovascularC-reactive proteininflammatory markermetabolic syndromeobesity


Metabolic syndrome (MetS) refers to a group of metabolic risk factors associated with the increased risk of cardiovascular diseases (CVDs) and type 2 diabetes,[] these factors include abdominal obesity, hyperlipidemia, hypertension, hyperglycemia, and insulin resistance.[,] The prevalence of MetS increases with age from lower than 10% in young adults to nearly 40% in people over 60.[] It is estimated that 20–25% of the world adult population suffers from MetS disorders. MetS is more prevalent in Asian population. There has been growing evidence suggesting that the inflammatory markers are the main causes of macro- and microvascular, including renal, ophthalmic, and cardiac, complications in patients with MetS who suffer from diabetes.[] The plasma concentration of C-reactive protein (CRP), a marker of inflammation, is elevated in obese patients, and is correlated with the MetS and decreases with weight loss. CRP is produced by mature adipocytes in adipose tissue and may contribute to the elevated circulating plasma CRP concentrations present in obese patients and people with the MetS. Treatment of the MetS is aimed at improving insulin resistance through lifestyle changes, namely weight loss and regular physical activity. In patients with abnormal glucose concentrations, dyslipidemia, or hypertension, treatment of the individual components of the syndrome may result in greater impact on reducing overall CVD risks. Given the prevalence of the MetS and the exaggerated CVD risks, innovative therapeutic approaches continue to evolve.[]

Studies have shown that even in patients without diabetes, each of the MetS’ risk factors, such as obesity, can increase inflammatory markers’ levels and cardiovascular adverse events.[,,] Ceriello and colleagues have shown that postprandial hyperglycemia and/or hypertriglyceridemia are associated with an increase of plasma levels of nitrotyrosine and inflammatory and thrombogenic biomarkers such as IL-6, soluble intercellular adhesion molecule (ICAM-1), soluble vascular cell adhesion molecule-1 (VCAM-1), and prothrombin fragment 1 + 2.[,,] They showed that postprandial dysmetabolism was accompanied by oxidative stress and endothelial dysfunction in diabetic patients as well.

Many antidiabetic medications are only effective in glycemic control and have slight or no effect on inflammatory markers and cardiovascular adverse events.[,] Acarbose is an alpha-glucosidases inhibitor; a group of antidiabetic agents which are poorly absorbed. Acarbose is associated with lesser gastrointestinal side effects compared to other alpha-glucosidase inhibitors and was used as a single drug or in combination with other antidiabetic medications to control blood glucose levels in type 2 diabetic patients. Acarbose can lower HbA1C level by 0.5–1% and can reduce the incidence of type 2 diabetes in prediabetic patients by 36%.[] This medication can reduce serum lipid levels, body weight, and blood pressure, and also decrease inflammatory markers and cardiovascular complications.[,,] This study aims to compare the effect of acarbose and placebo on inflammatory markers and cardiovascular indexes in MetS patients among Iranian population.


This double-blind randomized clinical trial registered in the Iranian Registry of Clinical Trials with the code IRCT20130924014752N5. The research population included all the patients with MetS referred to Isfahan Endocrine and Metabolism Research Center between August 2016 and August 2017. Among them, 84 patients with MetS based on American Heart Association criteria[] and endocrinologist’s opinions were selected using nonrandom convenience sampling method. The patients were evaluated regarding the height and weight and after calculating BMI (BMI = weight/height2, weight [kg] and height [cm]) and the cases with BMI greater than or equal to 30 kg/m2 were included. Patients with the history of underlying diseases such as respiratory diseases and rheumatoid arthritis, those taking antidiabetic or lipid-lowering medication over the past year, using low-calorie diet to reduce weight over the past year, and patients with a history of drug abuse or cases of unwillingness to continue the study of intolerance of high drug dosage and complications were excluded from the study. After obtaining written consent from qualified patients, they were divided into two groups of 42 patients receiving acarbose and placebo using random allocation software.

At baseline, demographic information such as age, sex, and BMI as well as metabolic parameters including body weight and waist circumference (WC), fasting blood sugar (FBS), triglyceride (TG), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), CRP marker, and cardiovascular markers including flow-mediated dilation (FMD), intima-media thickness (IMT), and epicardial fat thickness (EFT) were measured and recorded. FMD; IM and pericardial fat thickness were measured via two-dimensional M-mode echocardiography. Endothelial function was assessed as FMD at the brachial artery. It should be noted that cardiovascular markers were measured by a cardiologist using Doppler ultrasonography .

For patients in the acarbose group, treatment was initiated with 25 mg/day acarbose in the first week; and if the dosage was safe and well-tolerated, it was increased by 25 mg/day every week to a maximum dose of 100 mg/day within a month. The dosage was increased up to the maximum dose of 300 mg/day for 3 months and maintained for the second 3 months (a total of 6 months). Patients in the control group also received placebo in the same manner and they took these medications with their main meal to reduce gastrointestinal complications.

Response to treatment was considered if at least 5% of weight loss was achieved during the 6-month follow-up period, but if the patients had serious complications, they were excluded from the study. There were no severe drug side effects such as dehydration or elevated creatinine level. Only 10 patients were excluded from the acarbose group due to mild complications such as abdominal bloating, diarrhea and stool softening, and intolerance to increased drug dosage or unwillingness to continue the participation [Figure 1].

What are the preventative care for diabetes?

[1]Khalili N, Safavipour A. Evaluation of the Effects of Acarbose on Weight and Metabolic, Inflammatory, and Cardiovascular Markers in Patients with Obesity and Overweight. Int J Prev Med. 2020 Sep 5;11:140. doi: 10.4103/ijpvm.IJPVM_229_19


1. Limberg JK, Morgan BJ, Schrage WG. Peripheral blood flow regulation in human obesity and metabolic syndrome. Exerc Sport Sci Rev. 2016;44:116–22. [PMC free article] [PubMed[]
2. Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ, et al. American association of clinical endocrinologists and American college of endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract. 2017;23(Suppl 2):1–87. [PubMed[]
3. Han TS, Lean ME. A clinical perspective of obesity, metabolic syndrome and cardiovascular disease. JRSM Cardiovasc Dis. 2016;5:2048004016633371. [PMC free article] [PubMed[]
4. Verma P, Srivastava RK, Jain D. Association of lifestyle risk factors with metabolic syndrome components: A cross-sectional study in Eastern India. Int J Prev Med. 2018;9:6. [PMC free article] [PubMed[]
5. Lau DC, Yan H, Dhillon B. Metabolic syndrome: A marker of patients at high cardiovascular risk. Can J Cardiol. 2006;22:85B–90B. [PMC free article] [PubMed[]
6. Esser N, L’Homme L, De Roover A, Kohnen L, Scheen AJ, Moutschen M, et al. Obesity phenotype is related to NLRP3 inflammasome activity and immunological profile of visceral adipose tissue. Diabetologia. 2013;56:2487–97. [PubMed[]
7. Yamagishi S. Cardiovascular disease in recent onset diabetes mellitus. J Cardiol. 2011;57:257–62. [PubMed[]
8. Agrawal NK, Kant S. Targeting inflammation in diabetes: Newer therapeutic options. World J Diabetes. 2014;5:697–710. [PMC free article] [PubMed[]
9. Ceriello A, Giacomello R, Stel G, Motz E, Taboga C, Tonutti L, et al. Hyperglycemia-induced thrombin formation in diabetes: The possible role of oxidative stress. Diabetes. 1995;44:924–8. [PubMed[]
10. Esser N, Paquot N, Scheen AJ. Anti-inflammatory agents to treat or prevent type 2 diabetes, metabolic syndrome and cardiovascular disease. Expert Opin Investig Drugs. 2015;24:283–307. [PubMed[]
11. Younk LM, Lamos EM, Davis SN. Cardiovascular effects of anti-diabetes drugs. Expert Opinion on Drug Safety. 2016;15:1239–57. [PMC free article] [PubMed[]
12. Singla RK, Singh R, Dubey AK. Important aspects of post-prandial antidiabetic drug, acarbose. Curr Top Med Chem. 2016;16:65–70. [PubMed[]
13. Yamagishi S, Nakamura K, Takeuchi M. Inhibition of postprandial hyperglycemia by acarbose is a promising therapeutic strategy for the treatment of patients with the metabolic syndrome. Med Hypotheses. 2005;65:152–4. [PubMed[]
14. Tsai SS, Chu YY, Chen ST, Chu PH. A comparison of different definitions of metabolic syndrome for the risks of atherosclerosis and diabetes. Diabetol Metab Syndr. 2018;10:5613. [PMC free article] [PubMed[]

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