STUDY OF THE EFFECT OF

ACARBOSE AND VOGLIBOSE IN

TYPE-2 DIABETES MELLITUS
PATIENTS

MD JAWED AKHTAR
FINAL YEAR PG STUDENT
PMCH PATNA
INTRODUCTION
• Diabetes Mellitus is a group of metabolic disorder characterized by hyperglycemia
resulting from defects in insulin secretion, insulin action or both. Depending upon
the etiology of Diabetes Mellitus (DM), factors contributing to hyperglycemia
includes reduced insulin secretion, defective insulin action, decreased glucose
utilization and increased glucose production. The metabolic dysfunction associated
with DM cause secondary pathophysiologic changes in multiple organ system that
impose a tremendous burden on the individual with Diabetes Mellitus and on
health care system of the state.
• As per recent data published by International Diabetes Federation (IDF) World
atlas 2011,worldwide population affected with Diabetes Mellitus in 1995 was
135.3 million, and it has been showing a progressively increasing trend to 366.2
million people having Diabetes Mellitus in 2011.It is estimated that this will have
risen to 552 million by 2030. In India population affected is currently around 42.2
million and is expected to rise to 80 million by 2030 unless urgent preventive steps
are taken.
AIMS AND OBJECTIVES
 The main and objective of this research work is to observe and compare the effect
of Acarbose (25 mg) orally TDS with meals and Voglibose (0.20 mg) orally TDS with
meals in Type -2 Diabetes Mellitus patients as regards its efficacy and safety.
The parameters which have been used in this study for comparison of effect
between these two drugs are as follows :-
a) Fasting Plasma Glucose (FPG) and Post Prandial
Glucose (PPG).
b) HbA1c at 0 week and at the end of 24 th week.
c) Serum lipid profile which includes :-
• LDL-C.
• HDL-C.
• VLDL.
• Triglyceride.
• Total cholesterol.
d) Haemoglobin (Hb).
e) Total leucocyte count (TLC).
f) Serum Glutamic Pyruvic Transaminase (SGPT).
g) Serum Creatinine.
REVIEW OF LITERATURE
 CLASSIFICATION OF DIABETES
MELLITUS
1) Type1 Diabetes Mellitus: ( β-cell destruction,usually leading to absolute insulin
deficiency)
a) Immune mediated.
b) Idiopathic.
2) Type 2 Diabetes Mellitus (may range from predominantly insulin resistance
with relative insulin deficiency to a predominantly insulin secretory defect with
insulin resistance)
3) Other specific types of diabetes;-
A) Genetic defect of β cell function characterized by
mutation in:-
Hepatocyte nuclear transcription factor
(HNF) 4α (MODY 1).
• Glucokinase (MODY 2).
• HNF-1α (MODY-3).
• Insulin Promoter Factor (IPF) (MODY-4).
• HNF-1β (MODY-5).
• Mitochondrial DNA.
• Proinsulin or insulin conversion
 CLASSIFICATION OF DIABETES MELLITUS
B) Genetic defect in insulin action. Somatostatinoma.
Type A insulin resistance . Aldosteronoma.
Leprechaunism. Others.
Rabson-Mendenhall syndrome. E) Drug or chemical induced
Lipodystrophy syndrome. Vacor.
C) Disease of exocrine pancreas:- Pentamidine.
Pancreatitis. Nicotinic acid.
Trauma /Pancreactectomy. Glucocorticoids.
Neoplasia. Thyroid hormone.
Cystic fibrosis. Diazoxide.
Hemochromatosis. Beta-adrenergic agonists.
Fibrocalculous pancreatopathy. Thiazides.
Others. Dilantins.
D) Endocrinopathies :- α-interferon.
Acromegaly. Others.
Cushing’s syndrome. F) Infections:-
Glucagonoma. Congenital rubella.
Pheochromocytoma. Cytomegalovirus.
Hyperthyroidism. Others.
 CLASSIFICATION OF DIABETES MELLITUS

G. Other genetic syndromes associated with diabetes :-

Down's syndrome.
Klinefelter's syndrome.
Turner's syndrome.
Wolfarm's syndrome.
Friedreich ataxia.
Huntington's chorea.
Laurence-Moon- Biedl syndrome.
Porphyria.
Prader-willi syndrome.
Others.
 DIAGNOSIS OF DIABETES MELLITUS
1.FPG ≥126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake
for at least 8h*.
OR
2. Symptoms of hyperglycemia and a casual plasma glucose ≥200
mg/dl (11.1 mmol/l). Casual is defined as any time of the day
without regard to time since last meal. The classic symptoms of
hyperglycemia include polyuria, polydipsia, and unexplained weight
loss.
OR
3. 2-h plasma glucose ≥200 mg/dl (11.1 mmol/l) during an Oral
Glucoe Tolerence Test (OGTT). The test should be performed as
described by the World Health Organization, using a glucose load
containing the equivalent of 75 g anhydrous glucose dissolved in
water.*
* In the absence of unequivocal hyperglycemia, these criteria should
be confirmed by repeat testing on a different day.
 RISK FACTOR FOR TYPE 2 DIABETES MELLITUS
1. Family history of Diabetes Mellitus (i.e. parents or
siblings with Type 2 Diabetes Mellitus)
2. Obesity (BMI ≥ 30 Kg/m2 ).
3. Age ≥ 45yrs.
4. Race / ethinicity (e.g. African American,Hispanic American ,
Native American , Asian American,Pacific Islander ).
5. Previously identified IFG or IGT.
6. History of GDM or delivery of baby over 9 lbs.
7. Hypertension ( blood pressure ≥ 140/90).
8. HDL cholesterol level ≤ 0.90 mmol/L (35 mg/dl) and /or
triglyceride level ≥2.82 mmol/L ( 250 mg /dl).
9. Polycystic ovarian syndrome.
 COMPLICATIONS:
A) Acute complications:-
i) Diabetic ketoacidosis.
ii) Hyperglycemia hyperosmolar state.
iii) Hypoglycaemic –drug induced.
B) Chronic complications:-
i) Microvascular :-
Eye disease:- Retinopathy ( nonproliferative /proliferative ), macular edema.
Neuropathy :- Sensory and motor ( mono and poly neuropathy), autonomic neuropathy.
ii) Macrovascular :-
Coronary artery disease.
Peripheral artery disease.
Cerebrovascular disease.
iii) Metabolic complications :-
Diabetic dyslipidemia.
iv) Others:-
Gastrointestinal ( gastroparesis, diarrhoea).
Genito urinary ( uropathy / sexual dysfunction ).
Dermatologic.
Cataract.
Glucoma.
Periodontal disease.
INSULIN RESISTANCE SYNDROME OR SYNDROME X:-
The insulin resistance condition comprises a spectrum of disorders ,
with hyperglycemia representing one of the most readily diagnosed
features.
The syndrome X is used to describe a constellation of metabolic
derrangements that include insulin resistance ,hypertension
,dyslipidemia (low HDL and elevated triglycerides ),central and visceral
obesity, Type 2 Diabetes Mellitus or IGT/IFG and accelerated
cardiovascular disease.[11]
Clinical features of insulin resistance include;-
a) Abdominal obesity.
b) Acanthosis nigricans.
c) Hypertension.
d) Dyslipidemia.
e) Hyperuricemia.
f) Coagulation system abnormalities.
g) Impaired glucose tolerance.
h) Hyperinsulinemia.
 DIABETIC DYSLIPIDEMIA
ABNORMALITIES IN TYPE 2 DIABETES MELLITUS:
The characteristic pattern of lipid abnormalities in patients with Diabetes Mellitus consists of
moderate elevation in triglycerides, low High-Density Lipoprotein (HDL),cholesterol values, and an
increase in small dense Low-Density Lipoprotein (LDL) particles .This lipoprotein pattern is present
even before the onset of Diabetes Mellitus and is strongly associated with insulin resistance.The
small dense LDL particles are more intrinsically atherogenic because of their enhanced
susceptibility to oxidative modification and are less readily cleared from the circulation.LDL
cholesterol levels in patients with Type 2 Diabetes Mellitus are generally similar to those found in
the general population.

PATHOGENESIS :-
The origin of dyslipidemia in Diabetes Mellitus are complex but derive from specific abnormalities
in lipoprotein metabolism and abnormalities in insulin action . An increased flux of free fatty acids
to the liver, which is associated with insulin resistance and abdominal obesity, has been implicated
in the enhanced production of large very low density lipoprotein (VLDL) by the liver, the secretion
of which is not suppressed by meal-related insulin surges as it normally is in the insulin-sensitive
state. In addition to VLDL overproduction, reduced lipoprotein lipase activity and apolipoprotein
(apo) C-III enrichment of VLDL may retard VLDL and remnant clearance.
The accumulation of triglyceride-rich lipoproteins, coupled with the heightened action of
cholesteryl ester transfer protein, leads to an increased exchange of triglyceride for cholesterol
between VLDL and HDL and between VLDL and LDL particles. Hydrolysis of triglyceride-enriched LDL
and HDL by hepatic lipase, also considered to be upregulated in Type 2 Diabetes Mellitus, results in
the formation of small, cholesterol-poor HDL and LDL particles.
In addition, apo A-I may dissociate from triglyceride-enriched HDL. Free apo A-I is cleared rapidly
from plasma by excretion through the kidney, further reducing the availability of HDL for reverse
cholesterol transport.
 TREATMENT GOALS
Treatment Goals for Adults with Diabetes Mellitus
As recommended by the American Diabetes Association (ADA)
INDEX GOALS

Glycemic control(HbA1c) ≤ 7.0mmol/L

Pre-prandial capillary plasma glucose ≤ 5.0-7.2mmol/L

( 90-130 mg/dl)

Peak post-prandial capillary plasma glucose. ≤10.0 mmol/L

( 180 mg/dl)

CRP(C-REACTIVE PROTEIN) ≤ 3.0 mg/L.

LIPIDS

Total cholesterol 232.6

(mg/dl)

HDL(mg/dl) 36

Triglycerides 239.6
(mg/dl)
 PHARMACOLOGICAL MEASURE:-
ORAL ANTIDIABETIC AGENTS
A.Enhances Insulin secretion

1.Sulfonylureas (KATP Channel blocker)

First generation: Tolbutamide.
Second generation: Glibenclamide(Glyburide),Glipizide,Gliclazide
Glimepiride.
2.Meglitinide/phenylalanine analogues: Repaglinide,Nateglinide.
3.GLP-1 receptor agonists:Exenatide,Liraglutide.
4.DPP-4 inhibitors: Sitagliptin,Vildagliptin,Saxagliptin,Alogliptin
B.Overcomes Insulin resistance

1. Biguanides (AMPK activator): Metformin.

2. Thiazolidinediones (PPAR-Ƴ activator): Pioglitazone

C. Miscellaneous antidiabetic drug

1.α-Glucosidase inhibitor: Acarbose,Miglitol,Voglibose.
2. Amylin analogue: Pramlintide.
3. Dopamine-D2 receptor agonist: Bromocriptine.
4. Sodium- glucose cotransport-2( SGLT 2) inhibitor: Canagliflozin, Dapagliflozin
ACARBOSE
 ACARBOSE
• MECHANISM OF ACTION
Acarbose inhibits enzyme (glycoside hydrolases) needed to digest carbohydrates , specifically,alpha-
glucosidase enzyme in the brush border of the small intestine and pancreatic alpha-amylase.Pancreatic
alpha-amylase hydrolyzes complex starches to oligosaccrides in the brush border of the small
intestine,whereas the membrane-bound intestinal alpha-glucosidase hydrolyze oligosaccride,trisaccaride
and disaccharide to glucose and other monosaccride in the small intestine.Inhibition of these enzyme
systems reduces the rate of digestion of complex carbohydrates . Less glucose is absorbed because the
carbohydrate are not broken down into glucose molecules.
PHARMACOKINETICS STUDY
Acarbose is minimally absorbed in unchanged form and has extremely limited systemic
availability i.e .5 to 1.7 %.

DOSING
Since Acarbose prevents the digestion of complex carbohydrates , the drug should be taken
at the start of main meal ( taken with first bite of meal ) .Moreove, the amount of complex
carbohydrates in the meal will determine the effectiveness of acarbose in decreasing post
Prandial hyperglycemia . Adults may take doses of 25 mg 3 times daily, increasing to 100 mg
3 times a day.
SIDE EFFECT

1. Gastrointestinal distress , 2. Elevation of hepatic transaminase , 3. Reduction in haematocrit in some

patients
VOGLIBOSE
 VOGLIBOSE
• MECHANISM OF ACTION
Voglibose is one of the most important alpha glucosidase inhibitor it delays the digestion
and absorption of carbohydrates, thereby inhibiting Post Prandial Hyperglycemia and
hyperinsulinemia . Another reported advantage of Voglibose is that they decrease Post
Prandial glucose level without inducing hypesecretion of insulin.
• Pharmacokinetics[61]
Absorption:
Voglibose is poorly absorbed after oral administration. However, systemic adverse
effects have been observed.
Metabolism
the metabolism of Voglibose in liver is negligible.
Excretion
The renal excretion is negligible and plasma concentrations after oral dose have been
undetectable.
SIDE EFFECTS
1. Gastro Intestinal Tract, 2. show a rise in liver enzymes , 3. . Central Nervous System
effects.
MATERIALS AND METHODS
 MATERIALS AND METHODS
• The present prospective study includes evaluation of a total of 60 patients of Type 2 Diabetes
Mellitus attending outpatient department of Patna Medical College and Hospital, Patna ,Bihar
during the year 2016-2018 .The selection of patients was made on the basis of blood sugar
report(fasting and post prandial) or previous diagnosis of diabetes mellitus on OGTT or fasting and
post prandial blood sugar report.
ETHICS APPROVAL
Permission from ethics committee of Patna Medical College was obtained prior to initiation of the
study. Written informed consent was obtained from all the patients included in the study. In the
initial visit patients were counselled and were informed verbally in local language regarding the
purpose of the study, aims and objectives as well as risks and benefits along with responsibilities as
a participant. They were supplied with the informed consent form, and were instructed to read the
document carefully and to discuss with their family members before taking any decision regarding
participation.
PROTOCAL OF THE STUDY
Sixty patients of Type-2 Non Insulin Dependent Diabetes Mellitus uncontrolled by lifestyle
modification and dietary restrictions will be included in our study.They will be randomly divided
into two groups- Group A and Group B having 30 patients in each group. Group A will be given
Acarbose in a dose of 25 mg three times daily orally with meal. Group B will be given Voglibose in a
dose of 0.2 mg three times daily orally with meal. The study period for each group will be for 24
weeks.

Follow up will be done at 6 weeks,12weeks,24 weeks and adverse events will be recorded and
blood samples collected for estimation of HbA1c,Fasting plasma glucose,Post Prandial Glucose level
(after breakfast) and Lipid Profile .Determination of efficacy parameter will be done at 6wks,12wks
and 24 wks.

Inclusion criteria
a) Type-2 Diabetes Mellitus(Non
Insulin Dependent Diabetes
Mellitus) patients uncontrolled
by Lifestyle modification and
Dietary restriction.
b) HbA1c 7 to 9%.
c) 35 to 70 years of age.
d) Duration of Diabetes Mellitus
more than three months.
e) Body mass index(BMI) less than
35.
f) Both sexes.
Exclusion criteria
a) Patients with known hypersensitivity to
Acarbose and Voglibose.
b) Patients who are on current Insulin therapy or
have received Insulin for more than 6 weeks in
last 3 months.
c) Patients who are on chronic medication known to
affect glucose metabolism.
d) Patients with renal disease,Cardiac
disease,Hepatic insufficiency or Febrile
infection.
e) Alcoholics
f) Pregnant and lactating women.
g) Patients with Severe disturbance of
hematopoietic system .
h) Patients with Malignant tumours.
i) Patients with Inflammatory Bowel Disease,
Colonic ulceration, Partial Intestinal
Obstruction(or predisposed to intestinal
obstruction),Chronic Intestinal Disease.
j) Patients with Diabetic Ketoacidosis .
 STATISTICAL ANALYSIS

• Statistical analysis of various data so compiled

were finally carried out by standard methods Viz.
Simple mean, Standard deviation (SD),Standard
error (SE) and P values and Student test. Data
obtained during study were recorded in tabular
forms and were analysed by standard statistical
methods. Wherever necessary, he results were
depicted in the form of tables. Statistical tools
like MS Excel 2007 and MS Word 2007 have been
used to calculate the mean, SD and percentages
and generate graphs, tables, etc.
OBSERVATION AND RESULTS
 OBSERVATION AND RESULTS
The present study was conducted on a total 60
patients who were divided into two groups.
• Group A :- Consists of 30 patients subjected to
Acarbose mono-therapy in a dose of 25 mg three
times daily orally with meal.
• Group B :- Consists of 30 patients subjected to
Voglibose mono- therapy in a dose of 0.2 mg
three times daily orally with meal.
Out of 30 patients subjected to Acarbose therapy
18 were male and 12 were female.Out of 30
patients subjected to Voglibose therapy 20 were
male and 10 female.
 OBSERVATION AND RESULT

TABLE 1 TABLE 2
 20

18

TABLE 2- NO.OF PATIENTS

16

The table shows

maximum no. of 14

Diabetes Mellitus 12

patients 26(43.3%) 10 MALE

to be in the 6th 8
FEMALE

decade and least

no 1(1.6%) to be in 6

≤ 40 years. 4

0
< 40 41 - 50 51 - 60 61-70
OBSERVATION AND RESULT

PERCENTAGE

POLYURIA

NOCTURIA
8.32 POLYDIPSIA
15 10
POLYPHAGIA
13.33 21.67 30
RECURRENT UTI

PARATHESIAS
28.33
66.67 PERPHERAL
NEUROPATHY
31.67 DECREASED VISION

21.67 26.67 DELAYED WOUND

HEALING
HAEMODYNAMIC VARIABLES OBSRVED WITH ACARBOSE MONOTHERAPY

140

120

100 SBP

80 DBP

HR
60

40

20

0
BASELINE 6TH WEEK 12TH WEEK 24TH WEEK
HAEMODYNAMIC VARIABLES OBSERVED WITH VOGLIBOSE MONOTHERAPY

140

120

100
SBP

80
DBP

HR
60

40

20

0
BASELINE 6TH WEEK 12TH WEEK 24TH WEEK
PLASMA SUGAR LEVEL OF PATIENTS TREATED
WITH ACARBOSE MONOTHERAPY HbA1C VALUES
250
HbA1c
8.1

200 8

7.9

150 7.8

FPG 7.7
PPG
HbA1c
100 7.6

7.5

50 7.4

7.3

0 7.2
BASELINE 6TH WEEK 12TH WEEK 24TH WEEK BASELINE 24TH WEEK
PLASMA GLUCOSE LEVEL OF A PATIENTS
TREATED WITH VOGLIBOSE MONOTHERAPY. HbA1C VALUES
250
HbA1c
8.1

200
8

7.9
150 FPG
7.8

PPG
7.7
HbA1c
100
7.6

7.5
50

7.4

0 7.3
BASELINE 6TH WEEK 12TH WEEK 24TH WEEK BASELINE 24TH WEEK
 LIPID PROFILE OF PATIENTS TREATED
WITH ACARBOSE MONOTHERAPY
250 250

200 200
TG TG

TC
TC
150 150
LDL

LDL
VLDL

100 VLDL 100

HDL

HDL

50 50

0 0
BASELINE 6TH WEEK 12TH WEEK 24TH WEEK BASELINE 6TH WEEK 12TH WEEK 24TH WEEK
 LIPID PROFILE OF PATIENTS TREATED WITH
VOGLIBOSE MONOTHERAPY
250 250

200 200

TG
TG
TC
TC
150 150
LDL
LDL

VLDL VLDL
100 100
HDL HDL

50 50

0 0
BASELINE 6TH WEEK 12TH WEEK 24 TH WEEK BASELINE 6TH WEEK 12TH WEEK 24TH WEEK
DISCUSSION
 DISCUSSION
• Diabetes Mellitus is a metabolic disorder . The cardinal features is sustained
hyperglycaemia due to absolute or relative deficiency of insulin.
• There are many acute and chronic complications of this disorder. Chronic complications may
take years to develop still it is desirable to maintain the blood glucose of Diabetic patients at
normal levels if it is possible to do so safely.( Siperstein et al,1977) .[79]
• Acarbose is a α-Glucosidase Inhibitor an antidiabetic agent that competitively inhibits internal
brush border alpha-glucosidase in small intestine which hydrolyse sucrose and intermediate
starches. It binds reversibly and with high affinity to the carbohydrates and delay absorption
throughout small intestine and in upper part of jejunum. This results in significant reduction
in fasting and Post- Prandial Blood Glucose level. On the other hand Voglibose delays the
digestion and absorption of carbohydrates, thereby inhibiting Post Prandial Hyperglycemia
and hyperinsulinemia. Another reported advantage of Voglibose is that they decrease Post
Prandial glucose level without inducing hypesecretion of insulin.
• In the present study 60 Patients of Type 2 Diabetic Mellitus were studied. The patients were
divided into 2 groups, Group A (Acarbose) and Group B ( Voglibose) having 30 patients in
each. Group A was given Acarbose in a dose of 25 mg three times daily orally with
meal.Group B was given Voglibose in a dose of 0.2 mg three times daily orally with meal each
for 24 weeks.
• Follow up done at 6 weeks,12weeks,24 weeks where adverse event will be recorded and
blood samples collected for HbA1c,Fasting plasma glucose,Post prandial glucose level (after
breakfast) as well as Lipid Profile estimation.Determination of efficacy parameter was done at
6wks,12wks and 24 wks .
 SYMPTOMS AND SIGNS
• Polyuria and polydipsia were present in 26.67 % and 31.67 % of cases. The symptoms
subsided after adequate glycemic control.
• Peripheral neuropathy was present in 15 % of cases. The observation was based on altered
sensation and or impaired deep tendon reflexes especially the ankle jerk. About 21.6 % of the
patients had paresthesia.
• Ward et al (1971)[87] showed significant improvement in motor conduction velocity in the
median nerve after a period of 6 weeks of blood sugar control.
EFFECT ON LIPID PROFILE
• The serum lipid profile was investigated in both Groups at 0,6,12 and 24 weeks of study.
The serum lipid profile level in the Acarbose Group was TC-216, LDL-113.3,HDL- 35.6 ,VLDL-
55.1 ,TG- 230 mg/dl at 0 week and subsequently TC-196.13 ,LDL- 117.43, HDL- 40 ,VLDL- 46.5
,TG……210.93 mg/dl after 24 weeks.
• The serum lipid profile in Voglibose group was TC- 213.73, LDL- 108.83 ,HDL- 33.76 , VLDL-
52.6 ,TG- 227.2 mg/dl, at 0 week and subsequently to TC-196.37,LDL- 117.43 ,HDL- 37.33,
VLDL- 40.76,TG- 194.76, mg/dl after 24 weeks.
• The data was analysed statistically.The mean fasting, Post Prandial Plasma Glucose and serum
lipid profile after therapy was compared. Role of Acarbose in controlling lipid profile was
statiscally significant.Rise in HDL-C and reduction in triglycerides were seen.There was no
significant change in the value of LDL-C.
 Glycemic control
• The need to control hyperglycemia in Diabetic Patients is imperative. Αlpha-glucosidase
inhibitor competitively inhibits internal brush border alpha-glucose which hydrolyses sucrose
and intermediate starches in small intestine.It binds reversibly and with high affinity to the
carbohydrate attachment site of the alpha glucosidase. The digestion and absorption of
complex carbohydrates are delayed throughout small intestine rather than in upper part of
jejunum .This results in significant reduction infasting and Post Prandial Blood Glucose level .
Alpha- glucosidase inhibitors are widely used in the treatment of patients with Type 2
Diabetes Mellitus that have lowering effect on Post-Prandial Blood Glucose and insulin level
(Van de Laar et al,2005)[88]
• The response of plasma glucose level values with Acarbose monotherapy (Group A) and as
Voglibose monotherapy ( Group B) in Type 2 Diabetes Mellitus patients was evaluated.
• After 24 weeks therapy with Acarbose the mean Fasting Plasma Glucose (FPG) level in the
monotherapy group decreased from 140.27 mg/dl at 0 week to 130.4 mg/dl at 6
week,125.56 mg/dl at 12 week,after 24 week 122.86 mg/dl. The mean Post Prandial Plasma
Glucose was 231.33 mg/dl at 0 week which came down to 224.76 mg/dl at 6 weeks ,216.46
mg/dl at 12 weeks, 211.27 mg/dl at 24 weeks . The mean Fasting Plasma Glucose (FPG) level
in the Voglibose therapy group decreased from 136.17 mg/dl at 0 week ,124.57 mg/dl at 6
weeks, 123.8 mg/dl at 12 weeks after 24 weeks 125.1 mg/dl.The mean Post Prandial Glucose
(PPG) decreased from 227.13 mg/dl at 0 week,212.97 mg/dl at 6 weeks, 213.76 at 12 weeks,
after 24 weeks 210.6 mg/dl.
• After 24 weeks of therapy with Acarbose HbA1c level in Group A decreased from 8.001 % at
0 week to 7.51 % after 24 weeks . In Voglibose Group after 24 weeks of therapy, HbA1c level
in Group B decreased from 8.001 % at 0 week to 7.575 % .
SUMMARY AND CONCLUSION
 SUMMARY AND CONCLUSION

The present study was carried out in Patna Medical College and Hospital, Patna . The
study was carried out on patients attending Medicine outdoor and Diabetic clinic.
1. Sixty Type-2 Diabetes Mellitus patients with deranged lipid profile were chosen
and divided in two groups, Group A and Group B with 30 patients in each group
respectively.
2. Patients having Type 1 Diabetes Mellitus, heart disease, severe renal failure or
hepatic disease and those with normal lipid profile were excluded from the study.
3. Diabetes Mellitus was diagnosed on the basis of criteria issued by consensus
panels of experts from National Diabetic Group and WHO.
4. Fasting and Post Prandial Plasma glucose level were estimated initially at 0 week,6
weeks , 12 weeks , 24 weeks . Fasting serum samples were sent for estimation of
lipid profile at the start of study at 0 week , 6 weeks , 12 weeks and 24 weeks.
5. HbA1c was estimated at 0 and 24 weeks.
6. In the present study,Acarbose was given at a dose of 25 mg three times daily orally
with meal in Group A.Group B was given Voglibose in a dose of 0.2 mg three times
daily orally with meal each for 24 weeks.
Following conclusion were drawn from the present study
Clinical evaluation :
1. Maximum number of patients were in the sixth decade of life (26, 43.3%).
Minimum patients were in more than 70 years age group (2, 3.3%).
2. Males were approximately 2 times more than the number of female patients (68.3
% and 31.6 %) respectively.
The common presenting symptoms were as under
1. Weakness/fatigue 66.6%
2. Polydipsia 31.4%
3. Polyuria 24.07%
4. Polyphagia 25.9%
5. Weight loss 27.7 %
6. Paresthesia 20.3 %
7. Asymptomatic/ Diagnosed on
routine Check up 4.8 %
 Biochemical Evaluation
Acarbose monotherapy:- Group A
After 24 weeks of therapy with Acarbose the mean Fasting Plasma Glucose (FPG) level in Group A decreased
from 140.27 mg/dl at 0 week ,130.4 mg/dl at 6 weeks ,125.56 mg/dl at 12 weeks ,122.86 mg/dl at 24
weeks.
The mean Post Prandial Plasma Glucose was 231.33 mg/dl at 0 weeks ,224.76 mg/dl at 6 weeks ,216.46 mg/dl
at 12 weeks, 211.27 mg/dl at 24 weeks.
HbA1c at 0 week 8.001 % and 7.51 % at 24 weeks.
The mean serum lipid profile in this Group at 0, 6 ,12 , and 24 weeks therapy was also evaluated. The serum
lipid profile level in this group was TC-216, LDL -113.3,HDL-35.6 ,VLDL-55.1 ,TG-230 ,mg/dl at 0 week and
subsequently changed to TC -196.13 ,LDL-117.43 ,HDL-40 VLDL- 46.5 TG- 210.93 mg/dl after 24 weeks.
Voglibose monotherapy:- Group B
After 24 weeks of therapy with Voglibose the mean fasting plasma glucose (FPG) level in
Group A changed from 136.17 mg/dl at 0 week ,124.57 mg/dl at 6 weeks ,123.8 mg/dl
at 12 weeks ,125.1 mg/dl at 24 weeks.
The mean Post Prandial Plasma Glucose was 227.13 mg/dl at 0 weeks ,212.97 mg/dl at 6
weeks ,213.76 mg/dl at 12 weeks, 210.6 mg/dl at 24 weeks.
Level of HbA1c at 0 week 8.001 % and 7.575 % at 24 weeks.
The mean serum lipid profile in this Group at 0, 6 ,12 , and 24 weeks therapy was also
evaluated. The serum lipid profile level in this group was TC- 213.73, LDL-108.83 ,HDL-
33.76 ,VLDL- 52.6 ,TG- 227.2, mg/dl at 0 week which changed to TC-196.37 ,LDL- 117.43
,HDL- 37.33 VLDL- 40.76 TG- 194.36 mg/dl after 24 weeks.
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