1

The Metabolic Syndrome in the Elderly

(Potential Cardiometabolic Roles of ACARBOSE and GULOH-CISAR)

2008
09-750
Askandar Tjokroprawiro
Diabetes and Nutrition Center Dr. Soetomo Teaching Hospital
Airlangga University School of Medicine, Surabaya
An Overview: the Elderly MetS, GULOH-CISAR, and the Roles of Acarbose
The metabolic syndrome is a constellation of visceral fat obesity, impaired
glucose tolerance, atherogenic dyslipidemia, and increased blood pressure. The metabolic
syndrome is associated with a dysregulated adipose tissue; in part a consequence of
adipose cell enlargement and the associated infiltration of macrophages (Suganami et
al 2005). Adipose cell enlargement leads to a proinflammatory state in the cells with
reduced secretion of adiponectin and with increased secretion of several cytokines and
chemokines including TNF, interleukins (IL) such IL-6, IL-8, and MCP-1. The
recruitment of macrophages in to the adipose tissue is initiated by the presence of MCP-1.
The adipose lineages (preadipocytes and adipocytes) and macrophages share
numerous functional properties. Surprisingly, the preadipocyte profile is closer to the
macrophages than to the adipocyte profile. Charriere et al (2003) suggested
preadipocyte and macrophage phenotypes are very similar and that preadipocytes have
the potential to be very efficiently and rapidly converted into macrophages.
The increased release of cytokines mentioned above leads to impaired
differentiation of the preadipocytes with reduced induction of adiponectin and with
reduced lipid accumulation, thus promoting ectopic lipid storage through metastatic fat.
The metastatic fat may deposit in hepatocyte, pancreatic -cell, and muscle, hence,
insulin resistance may pursue. Furthermore, insulin resistance enhances both lipolysis and
proinflammatory state, because insulin has anti-inflammatory effects.
Abbreviations: AACE = American Association of Clinical Endocrinologists; ACS = Acute Coronary
Syndrome; ADMA = Asymmetric Dimethylarginine; AHA /NHLBI = American Hearth Association /
National Heart, Lung, and Blood Institute; ATP III = Adult Treatment Panel III; CHD = Coronary Heart
Disease; CMR = Cardiometabolic Risk; CVE = Cardiovascular Event; EGIR = European Group for Study
of Insulin Resistance; GULOH-CISAR = Glucose, Uric acid, Lipid, Obesity, Hypertension, Cigarette,
Inactivity, Stress, Alcohol, Regular checkup; IDF = International Diabetes Federation; INA = Indonesia;
LRD = Lifestyle Related Disease; MECAR = Metabolic Cardiovascular; NEFA = Non Esterified Fatty
Acid; NGT = Normal Glucose Tolerance; PPAR- = Peroxisome Proliferator-Activated Receptor-;
TNF = Tumor Necrosis Factor ; VAT = Visceral Adipose Tissue; WC = Waist Circumference
Temu Ilmiah Geriatri Semarang
Peningkatan Mutu Berfikir dan Kualitas Pelayanan Secara Holistik yang Profesional di Bidang Ilmu Geriatri
dan Gerontologi dalam Menghadapi Perkembangan Iptek dan Daya Saing di Era Global
Semarang, 28 30 Maret 2008
 2

Thus, metabolic syndrome is associated with a dysregulated adipose tissue

attributable to inflammation with increased levels of several proinflammatory molecules
or can be called inflamed adipose tissue (Gustafson et al 2007).
The metabolic syndrome (MetS) can be considered as preclinical stage of
cardiovascular diseases, and the MetS is located at the stage-3 of lifestyle related disease
(LRD) as mentioned below.
Excess weight and obesity (underlying cause of the MetS) increase the risk of
developing type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD), and they
are recognized as independent predictors of cardiometabolic risk (CMR) factors. The
MetS is a constellation of interrelated risk factors of metabolic that appear to directly
promote the development of atherosclerotic cardiovascular disease (ASCVD); patients
with the MetS are also at increased risk for developing T2DM.
The Emergence of the Metabolic Syndrome in the Elderly is shortly
described. According to Rethmann et al (2006), the metabolic syndrome affects between
25% and 50% of the elderly populations in Southern Germany depending on the
definition (WHO 1998, ATP-III 2001, or IDF 2005). The higher prevalence of the IDF-
defined metabolic syndrome most likely reflects both the lower cut offs for the abdominal
obesity and the larger importance given to this risk factor.
Based on both criteria ATP-III 2001 and IDF 2005 for the metabolic syndrome,
the prevalence of the metabolic syndrome increased strongly with age (Hildrum et al
2007) The IDF-2005 considered that visceral obesity is highly correlated with insulin
resistance (which was a core factor in the WHO 1998 definition, but cumbersome to
assess in clinical practice) and thus essential for diagnosis of the metabolic syndrome.
The IDF recommended, Management of the condition should be aggressive and
uncompromising in its aim to reduce the risk of cardiovascular disease and T2DM.
As reported in Korea by Kim et al (2007), there was an increased risk of the
metabolic syndrome with post menopausal status. A study in the US (Park et al 2003)
also demonstrated an increased risk of the metabolic syndrome among post menopausal
women. One study of 124 Argentine women reported that post menopausal women had a
22% higher prevalence of the metabolic syndrome than pre menopausal women (Mesch
et al 2006).
Estrogen promotes the accumulation of glute-femoral fat (Krotkiewski et al 1983),
and the loss of estrogen with menopause is associated with an increased in central fat
(Poehlman et al 1995) which may promote the occurrence of the metabolic syndrome.
This inter-correlated adverse change in metabolic risk factor justifies identification of
distinct menopausal metabolic syndrome which originates in estrogen deficiency and
which could contribute to the increased risk of coronary heart disease seen inpost
menopausal women.
In conclusion, estrogen replacement may diminish the expression of the
metabolic syndrome.
Recent data show that the decline of testosterone and daily amount of stress
contribute to the accumulation of visceral fat which is part of the metabolic syndrome or
can be called andropausal metabolic syndrome. Not only andropause and metabolic
syndrome are related, but higher testosterone levels are potentially preventive for
metabolic syndrome and CVD. Waist circumference (WC) of men is greatly influential to
 3

the development of the metabolic syndrome. Hence, the bigger belly (WC), the lower
the testosterone levels, and the higher the risk for the heart disease is.
Low testosterone level has been linked to insulin resistance and glucose level.
Also, many studies have confirmed that men with diabetes have the lowest of free
testosterone. Men with low levels of testosterone increased their triglycerides over the
day, which the men who had high levels of testosterone did not increase. In addition,
there a positive relation with high testosterone levels and higher HDL levels.
In conclusion, low levels of testosterone are close related with the manifestation
of the metabolic syndrome. Hence, testosterone replacement therapy may reduce the
expression of the metabolic syndrome. Villareal et al (2004) demonstrated that
replacement with hormone dehydroepiandrosterone (DHEA), that widely available as
dietary supplement without prescription, could play a role in prevention and treatment of
the metabolic syndrome associated visceral obesity.
The Endo-Metabolic Itinerary: Obesity the MetS CMR, and the CMDs
is briefly described as seen in FIGURE-1 (from Stage-1 to Stage-4). Based on clinical
experiences, the developmental evolution of LRD can be staged as follows: Stage-0
(healthy lifestyle), Stage-1 (westernized or unhealthy lifestyle), Stage-2 (abdominal
obesity), Stage-3 (the MetS, prediabetes, adolescent-obesity), and Stage-4 (ASCVD,
T2DM, adolescent T2DM, Stroke, Etc).
Chronologically, several criteria proposed for clinical diagnosis of the MetS can
be summarized and listed in this paper (TABLE-1): WHO (1998), EGIR (1999), ATP III
(2001), AACE (2003), IDF (April 2005), and AHA/NHLBI (July 2005).
The MetS, which affects about 40% of the population over 50 years old in the US
and nearly 30% in Europe, is a significant public health issue worldwide and one of the
major causes of ASCVD. The prevalence of the MetS (ATP III criteria) in individuals
(over 40) who underwent medical check up in Surabaya (Indonesia) was 32%, whereas it
was reported 43.3% in treated T2DM and 59.0% in nave T2DM; however, the
prevalence of the MetS (ATP III criteria) in obese patients with T2DM was 81.7%.
Regardless of diagnostic criteria used, therapeutic lifestyle change (TLC), with emphasis
on weight reduction, contributes first-line intervention for individuals with the MetS.
GULOH-CISAR, 10 (ten) practical guidelines for healthy life, will be shortly
described in this paper. In addition, treatment specifically targeting insulin resistance and
metabolic risk factors should be considered for patients with the MetS especially
postprandial hyperglycemia; hence, insulin resistance is the primary target of intervention
for the MetS. Certainly, weight reduction to decrease visceral fat accumulation or to shift
Stage-3 (the MetS) towards Stage-0 of LRD will reduce insulin resistance and
postprandial hyperglycemia.
Acarbose (Glucobay), an alpha glucosidase inhibitor, has potential
cardiometabolic properties with minimally 13 beneficial effects as shown in FIGURE-3.
Such 13 benefits can be listed below.
1. Improved restoration of endothelial dysfunction in prediabetes
2. Reduced risk to development of T2DM
3. Able to reverse to NGT (normal glucose tolerance)
4. Decreased systolic blood pressure
5. Decreased diastolic blood pressure
6. Reduced risk of new hypertension
 4

7. Reduced risk of CVD

8. Lowered postmeal insulin
9. Lowered postprandial hyperglycemia
10. Improved insulin sensitivity
11. Decreased fibrinogen in T2DM
12. Suppressed NF-kB activation
13. Decreased serum CRP in prediabetes

Six Criteria of the Metabolic Syndrome

Several organizations have attempted to formulate criteria for clinical diagnosis of
the MetS. The first proposal came in 1988 by Reaven (Syndrome X or the MetS-X), and
then chronologically (TABLE-1) followed by WHO (1998), EGIR (1999), ATP III
(2001), AACE (2003), IDF (April 2005), and finally AHA/NHLBI (July 2005) as seen in
(TABLE-3).
Importantly, the WHO (1998) group allowed the term metabolic syndrome to be
used in patients with T2DM who otherwise met the requirements for the syndrome. They
pointed out that patients with T2DM often have a clustering of ASCVD risk factors,
which puts them at particularly high risk for ASCVD (Alexander 2003, Ninomiya 2004).
In 1999, the European Group for Study of Insulin Resistance (EGIR) proposed a
modification of the WHO definition (Balkau, 1999). This group used the term insulin
resistance syndrome rather than metabolic syndrome. In 2001, the National Cholesterol
Education Program (NCEP) Adult Treatment Panel III (ATP III) criteria did not require
the existence of insulin resistance per se.
In 2003, the American Association of Clinical Endocrinologists (AACE) modified
ATP III criteria to refocus on insulin resistance as the primary cause of metabolic risk
factors (Einhorn, 2003). Like EGIR (Balkau, 1999), they used the name insulin resistance
syndrome. Major criteria were IGT, elevated triglyceride, reduced HDL-C, elevated blood
pressure, and obesity. No specified number of factors qualified for diagnosis, which was
left to clinical judgment.
In April 2005, the International Diabetes Federation (IDF) published new criteria
that again modified the ATP III definition (IDF, 2005). In this criteria, ethnic specific
values of waist circumference are listed (TABLE-2).
5
 6

Ethnic Specific Values of Waist Circumference (IDF 2005)

Central obesity is most easily measured by waist circumference using the
guidelines in TABLE-2 which are gender and ethnic-group (not country of residence)
specific. The consensus group acknowledges that these are pragmatic cut-points taken
from various different data sources and that better data will be needed to link these to risk.

TABLE-2 ETHNIC SPECIFIC VALUES OF WAIST CIRCUMFERENCE

(IDF 2005)
Country /Ethnic Group Waist Circumference*
Europids Male 94 cm
In the USA, the ATP-III Female 80 cm
values (102 cm male; 88
cm female) are likely to
continue to be used for
clinical purposes
South Asians Male 90 cm
Based on a Chinese, Malay Female 80 cm
and Asian-Indian
Population
Chinese Male 90 cm
Female 80 cm
Japanese Male 85 cm
Female 90 cm
Ethnic South and Central Use South Asian recommendations until more specific data
Americans are available
Sub-Saharan Africans Use European data until more specific data are available
Eastern Mediterranean and Use European data until more specific data are available
Middle East (Arab)
Populations
*) In future epidemiological studies of populations of Europid origin, prevalence should be given
using both European and North American cut-points to allow better comparisons.

Although a higher cut-point is currently used for all ethnic groups in the USA for clinical
diagnosis, it is strongly recommended that for epidemiological studies and, wherever
possible, for case detection, ethnic group specific cut-points should be used for people of
the same ethnic group wherever they are found. Thus, the criteria recommended for Japan
would also be used in expatriate Japanese communities, as would those for South Asian
males and females regardless of place and country of residence.
The American Hearth Association (AHA) / National Heart, Lung, and Blood
Institute (NHLBI) Scientific Statement, in contrast to IDF maintains the ATP III criteria
except for minor modifications (TABLE-3). The majority of these reports are supportive
of the present structure of ATP III criteria.
 7

To measure waist circumference (WC) according to AHA/NHLBI Scientific

Statement (Grundy et al 2005): locate top of right iliac crest. Place a measuring tape in
horizontal plane around abdomen at level of the iliac crest. Before reading tape measure,
ensure that tape is snug but does not compress the skin and is parallel to floor.
Measurement is made at end of a normal expiration.

Staging of Lifestyle Related Disease

Based on clinical experiences, the evolution of lifestyle related disease (5 Stages)
can be seen in FIGURE-1 9the endo-metabolic itinerary from obesity to the CMDs. The
previous two criteria for diagnosis of the MetS (WHO 1998 and ATP III 2001) have been
described in the previous papers, and the recent one (IDF criteria) is also built in
FIGURE-1.
 8

As seen in FIGURE-1, to shift Stage-3 towards Stage-0 with therapeutic lifestyle

change (TLC) as described in GULOH-CISAR (TABLE-4) is recommended as the
primary target of intervention for the MetS.

Ten Practical Guidelines for Healthy Life

As previously mentioned, TLC should be recommended as the primary target of
intervention for the LRD (the MetS, etc). On the basis of clinical experiences as seen in
TABLE-4, Ten Practical Guidelines for the Healthy Life (GULOH-CISAR = Glucose,
Uric acid, Lipid, Obesity, Hypertension, Cigarette, Inactivity, Stress, Alcohol, Regular
check up) can be used to push the Stage-2 , Stage -3, or Stage - 4 of LRD towards the
Stage-0.
 9

GULOH-CISAR (clinical experiences since 1995 which is almost annually renewed) is

the abbreviated items of ten (10) healthy guidelines to cope with abnormal Glucose blood
level, abnormal Uric acid blood level, and other components of GULOH-CISAR.

Abdominal Obesity and Its Consequences

The atherogenic link between abdominal (visceral) obesity and metabolic risk
factors will be briefly described. The increased metabolic risk can be largely attributed to
the fact that a high accumulation of abdominal adipose tissue, especially of visceral
adipose tissue (FIGURE-2) is strongly associated with 10 atherogenic components as
mentioned below (Desprs 2003).
Such components are sequently numbered by Tjokroprawiro (2004) as follows.
1. Increased fasting FFA 7. Normal LDL
2. Elevated apolipoprotein-B
8. Elevated small dense LDL : LDL < 1.2
3. Elevated remnant lipoprotein Apo-B
4. Elevated fasting triglycerides 9. Reduced HDL, Increased Small HDL
5. Elevated post prandial
10. Increased Chol./HDL-C ratio
triglycerides
6. Increased LDL
 10

The results of the Quebec Cardiovascular Study (Lamarche et al 1998) have provided
evidence that some features of the MetS including:

1. fasting hyperinsulinemia (as a crude marker of insulin resistance)

2. elevated Apo-B concentration (as a marker of the concentration of atherogenic
dyslipidemia
LDL
3. elevated small dense LDL particles (by using formula
Apo-B< 1.2)
Such factors mentioned above were predictive of substantially increased risk of ischemic
heart disease (IHD) in a sample of middle-age men followed by the occurrence of a first
IHD event over 5-year follow-up period.
The atherothrombotic, proinflammatory abnormalities in viscerally obese patients
have been summarized by Desprs in 2001 as seen in TABLE-5.

TABLE 5 Atherothrombotic, Proinflammatory Abnormalities in Visceral Obesity

(Desprs 2001, Provided: Tjokroprawiro 2004 - 2008)
The Cluster of Complications Substantially Increases the Risk of CHD in Affected Patients
1. Insulin Resistance 8. Small, dense, LDL and Smaller HDL particles
2. Hyperinsulinemia 9. Postprandial Hyperlipidemia
3. Glucose Intolerance 10. Hypertension
4. Type 2 Diabetes Mellitus 11. Impaired Fibrinolysis and Increased susceptibility to
5. Hypertriglyceridaemia thrombosis (raised PAI-1 and Fibrinogen)
6. Hypoalphalipoproteinaemia 12. Low Chronic Inflammation State
(raised IL-6, raised hsCRP, etc)
7. Increased Apo-B 13. Endothelial Dysfunction

Obese people with less visceral adipose tissue (VAT) were found to have normal
glucose tolerance when compared with lean controls (Pouliot et al 1992). Obese people
with a high accumulation of VAT, however, showed an increase in their glycemic
response to an oral glucose load which was measurably higher than that in obese people
with less VAT or in non-obese controls (Pouliot et al 1992); major differences were also
noted in the plasma insulin response to the oral glucose load. Thus, viscerally obese
people are at the highest risk of developing T2DM. The accumulation of VAT is
particularly assumed to play an important role in the etiology of the MetS, notably by the
overexposure of the liver to free fatty acids, which results in insulin resistance,
hyperinsulinemia, and atherogenic dyslipidemia as seen in FIGURE-2.
Waist circumference (WC) and waist-to-hip ratio (WHR) are widely used as
indicators of abdominal obesity in population studies (Bjrntorp 1991). Most of current
studies agree that WC is probably a better indicator of VAT than is WHR. Several studies
found WC to be a better marker of VAT and to correlate strongly with cardiovascular risk
factors than WHR. Waist circumference (WC) was found to be a simple but useful
correlation with the amount of VAT, and would help clinicians to identify individuals with
a high likelihood of having the features of the MetS (FIGURE-1). Therefore, WC can be
used as a good marker of visceral obesity, of atherogenic dyslipidemia, as well as insulin
resistance, prothrombotic and proinflammatory states (FIGURE-2). Desprs (2003) found
that the presence of hypertriglyceridemic waist (WC 90 cm combined with TG 180
 11

mg/dl) was practical and systematically predictive of a very high likelihood (~ 80%) of
finding features of the MetS. Hence, hypertriglyceridemic waist can be practically used
as a crude indicator of the presence of the MetS.

Potential Cardiometabolic Effects of Acarbose

Postprandial hyperglycemia is associated with an increased risk of cardiovascular
disease (CVD). The Diabetes Epidemiology Collaborative Analysis of Diagnostic Criteria
in Europe (DECODE) analyzed data from 28.549 individuals with and without T2DM for
11 years concluded that 2 hour post challenge plasma glucose (2hPG) levels were more
strongly associated with the risk of all-causes and cardiovascular morality than were
caries funding fasting plasma glucose (FPG) levels (DECODE 2001, 2003). A further
study showed that the risk of CVD associated with prediabetes is independent of future
progression to T2DM (Qiao et al 2003).
The similar study the Diabetes Epidemiology Collaborative Analysis of
Diagnostic Criteria in Asia (DECODA), support the results of DECODE Study. In
DECODA Study, 6.817 individuals of Asian origin were followed for 5-10 years
(Nakagemi et al 2004) and they showed that the risks of both all-cause and CVD
mortality significantly increased with increasing 2hPG levels (p <0.001),but no
significant differences in risk of mortality were seen with increasing FPG levels.
 12

In conclusions, postprandial hyperglycemia is associated with cardiovascular

mortality either in Europe (DECODE) or in Asia (DECODA).
The Euro Heart Survey (Bartink et al 2004) with 3.444 patients with coronary
artery disease (CAD) reported that overall, 75% of those patients had dysglycemia. The
similar survey, the China Heart Survey recruited 3.513 patients hospitalized for CAD (Hu
et al 2006). Of these patients, 33% had known T2DM based on a FPG test. OGTTs were
administered to the remaining patients. Overall, 77% of the patients had dysglycemia.
In conclusions, based on the results of DECODE (2001) and DECODA (2004),the
Euro Heart Survey (Barturk et al 2004), and the China Heart Survey (Hu et al 2006),
accumulating evidence suggest a close association between dysglycemia and CVD.
Ryden et al (2007) reported the European Society of Cardiology (ESC) and the
European Association for the Study of Diabetes (EASD) guideline for diabetes,
prediabetes, and CVD highlight the close relationship between dysglycemia and CVD,
encourage closer collaboration between diabetologists and cardiologists, and include
algorithm for diagnosing of dysglycemia and CVD in high risk patients.
Chiasson et al (2003) in the Study to Prevent Non-Insulin Dependent Diabetes
Mellitus (STOP-NIDDM) assessed the effects of acarbose (Glucobay) on the risk of
developing T2DM as a primary endpoint in 1.429 individuals with prediabetes. The study
revealed that acarbose showed several benefits as listed below.
a 36% relative reduction in the risk of developing T2DM (36% reduction,
p=0.0003 vs placebo, based on 2 OGTTs)
a 35% reversion to normal glucose tolerance (35% reduction, p<0.0001 vs
placebo)
a 49% reduction in the risk of a first CV event in individuals with prediabetes
(p=0.03 vs placebo)
in particular, a 91% reduction in the risk of clinical myocardial infarction (MI)
with p=0.02 vs placebo
these findings in a diabetes population are supported by similar results in patients
with T2DM.
significant reductions in systolic and diastolic blood pressure compared with
placebo; in particular, the risk of new cases of hypertension in acarbose treated
group was reduced by 34% (p=0.006)
The Meta analysis of Risk Improvement with Acarbose (MeRIA) analyzed data from 7
(seven) long term trials, and reported a 35% reduction in the risk of a first cardiovascular
event in patients receiving acarbose, with p=0.00061 vs placebo (Hanefeld et al 2004)

Summary
1. Studies in both Europe (DECODE2001, 2003) and Asia (DECODA 2004) have
confirmed the close association between postprandial hyperglycemia and CVD
2. The Euro Heart Survey (Bartink et al 2004) and the China Heart Survey (Hu et al
2006) reported the similar results that dysglycemia is common and often an
diagnosed in patients with CAD. Overall, three-quarters (+ 67%) of undiagnosed
T2DM had dysglycemia
3. ESC / EASD guidelines (Ryden et al 2007) recommend the integrated
management of dyslipidemia ( by diabetologists) and CVD (by cardiologists)
 13

4. In STOP-NIDDM (Chiassen et al 2003), acarbose (Glucobay) reduced the risk

of developing T2DM, the risk of first CV event in individuals with prediabetes,
both systolic and diastolic blood pressure, the risk of new hypertension. Acarbose
therapy was also associated with reversion from diabetes to normal glucose
tolerance (p<0.0001 vs placebo).

Taken together, there is growing interest in the cardiovascular benefits of

hyperglycemia therapies, such as acarbose.
The Acarbose Cardiovascular Evaluation (ACE) with the expected study
period 2007 2013 will investigate the effect of acarbose on the risk of a further
cardiovascular event in patients with established CVD and prediabetes.
Hence, the aim of ACE is to determine whether acarbose (Glucobay) can reduce
the CV-related morbidity and mortality of patients with established CVD and prediabetes.

The Study Design of ACE (2007 2013)

CVD and dysglycemia are global issues cardiologist and diabetologists should
work together to integrate the management of dysglycemia and CVD
Randomized, double-blind, placebo-controlled trial
Dosing : acarbose 50mg three times a day, placebo 50mg tid
Patients with established CVD and prediabetes
~ 7.500 patients
~ 150 centers in mainland China and Hong Kong
Minimum follow up of 4 years
Primary endpoints (composite): time to the first occurrence of cardiovascular
death, resuscitation cardiac arrest, non-fatal MI, or fatal or non-fatal stroke
Secondary endpoint: time to diagnoses of new-onset T2DM, and time to
occurrence of individual cardiovascular events or death.

Conclusions
1. ACE is the logical further investigation for integrated management of
dysglycemia and CVD
2. ACE will extend and be complementary with the results of STOP-
NIDDM,DECODE study, DECODA study, the Euro Heart Survey the China
Heart Survey, and the ESC / EASD guidelines-2001 for patients with diabetes,
prediabetes and CVD
3. The expected results of ACE study are most likely influential to the management
of prediabetes and CVD worldwide
4. The ACE is an exciting new study that will widely extend the understanding of
how to manage patients with established CVD and dysglycemia
5. On the basis of the previous description and the results of several studies,
acarbose can be prescribed as the first-line drug in the treatment of prediabetes
and CVD of elderly patients with metabolic syndrome.

The 13 Cardiometabolic Effects of Acarbose

 14

Based on the selected literature studies, the author summarized minimally 13

beneficial cardiometabolic effects of the acarbose as seen in FIGURE-3

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