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A Study of Dyslipidemia in Type 2 Diabetes

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 Original Research Article
A Study of Dyslipidemia in Type 2 Diabetes
Mellitus
Narasimhaswamy K N1, Ravi G N1, Neema K N2
Abstract:
Introduction: Diabetes is an “iceberg disease” affecting at least 347 million people in the world, with a prev-
alence of 10%. Type 2 Diabetes Mellitus, the commonest variety of diabetes, is characterized by either defi-
ciency of insulin or resistance to action of insulin or both. Insulin has important effects on key steps in the
metabolism of lipids and lipoproteins, which are altered in diabetes, possibly leading to dyslipidemia. Ob-
jective: The study was done to investigate association of obesity indices, lipid profile and blood glucose
levels with diabetes. Methodology: This is a case control study consisting of 60 (35males & 25 females) cases
& 60 age and sex matched controls, in the age group of 30-60 years. Participants fulfilling the inclusion and
exclusion criteria were included in the study. Obesity indices (i.e., body mass index, skin fold thickness,
waist hip ratio, and percentage fat in the body); lipid profile (including serum total cholesterol, triglyceride,
VLDL, LDL, and HDL Cholesterol) levels & blood glucose levels (Fasting & Post prandial) were investigated
in both the cases & controls. The values thus obtained were analysed by Student‘t’ test. Results: On com-
parison, plasma glucose levels, obesity indices, cholesterol, triglyceride, VLDL, LDL were significantly
higher (p<0.01) and HDL levels were significantly low in Type 2 Diabetes Mellitus cases as compared to
controls (p<0.01). Conclusions: By this study, we can conclude that obesity indices, cholesterol, Triglyceride,
VLDL, LDL were higher and HDL levels were low in Type 2 Diabetes Mellitus, which may be the cause for
increased incidence of coronary artery complications in type 2 diabetes.
Keywords: Type 2 Diabetes Mellitus, Dyslipidemia, Obesity Indices

INTRODUCTION
which often accompanies Type 2 METHODOLOGY
Diabetes Mellitus. Insulin has im- This study was conducted in
Diabetes is an “iceberg dis-
portant effects on key steps in the district hospital, Shimoga Institute
ease” affecting at least 61.4 million
metabolism of lipids and lipopro- of Medical Sciences, Shimoga,
people in India with a prevalence
teins, which are altered in diabe- from 2006 to 2008. 60 confirmed
of 12.4% & 347 million people
tes, possibly leading to cases of Type 2 Diabetes Mellitus
throughout the world with a Prev-
dyslipidemia. (35 males and 25 females) in the
alence of 10% of which 90% is type age group of 30 – 60 years and 60
This study was conceptualised
2 diabetes.1 In 2008, 1.2 million age and sex matched controls (35
to assesses and compare levels of
people died from consequences of males and 25 females) in the age
plasma glucose fasting and post
high blood sugar. Type 2 Diabetes group of 30-60 years were in-
meal, total serum cholesterol, tri-
Mellitus, the commonest variety of cluded in the study. The selection
glyceride, HDL, LDL and VLDL in
diabetes is characterized by either criteria for Type 2 Diabetes Melli-
control and Type 2 Diabetes Melli-
deficiency of insulin or resistance tus subjects was post prandial glu-
tus subjects. cose level < 200 mg% (controlled
to action of insulin or both. Insulin
resistance is also seen in obesity, diabetes).2
They had not received oral anti
diabetics, cholesterol lowering
1Department of Physiology, Adichunchanagiri Institute of Medical Sciences, agent, and hormones for one
B.G.Nagara, Mandya, Karnataka, India. 2Department of Biotechnology, Sri month. Controls had not suffered
Jayachamarajendra engineering college, Mysore. from diabetes, atherosclerosis,
Address for Correspondence: Dr Narasimhaswamy K N, Professor and Head, thrombotic disease, or IHD. No
Dept. of Physiology, Adichunchanagiri Institute of Medical Sciences, B.G.Nagara, subjects had a family history of di-
Mandya, Karnataka, India. abetes. None had history of smok-
email: neemaswamy@hotmail.com ing or had diseases such as
Nephropathy, Neuropathy or any
other complication of diabetes. All
were on mixed diet. Participants
International Journal of Health Information and Medical Research Vol: 1, Issue: 1, Jan 2014 12
after consenting to the study were 7. Waist/Hip ratio was meas- Data was tabulated using Mi-
instructed to take their dinner be- ured with simple tape at the levels crosoft Excel and analysed with
fore 10 PM and report for investi- of waist and hip of the subjects us- Epi-info software. Continuous
gations the next morning at 9 AM. ing a non-stretchable measuring data was analysed using students
The following investigations tape. t test and categorical data by Chi
were performed: 8. Fasting blood sample of Square test. Probability value less
1. Measurement of body mass about 8 ml from antecubital vein than 0.05 was considered signifi-
index, skin fold thickness and was collected in a glass syringe cant.
waist/hip ratio. thinly smeared with liquid paraf-
2. Estimation of fin. Two ml blood was transferred RESULTS
a. Fasting and Post Pran- to fluoride bulb containing so- 60 cases (35 males and 25 fe-
dial blood glucose. dium fluoride 10 mg/ml for blood males) and 60 age and sex
b. Serum Cholesterol. glucose estimation. Remaining matched controls included in the
c. Serum Triglyceride blood was transferred to plain study were also similar with re-
d. Serum HDL cholesterol bulb for estimation of serum cho- spect to religion, socio-economic
and lesterol, triglyceride and HDL status (p>0.05). Table 1 shows the
e. VLDL and LDL were es- Cholesterol. Post meal blood sam- significant obesity indices and
timated by computation. ple was collected 120 minutes after plasma glucose comparison be-
3. Body mass index was meas- the meal. Blood glucose estimation tween cases and controls. Table 2
ured by the formula: was done by GOD-POD i.e. glu- shows the comparison of lipid
4. BMI = Weight(Kg)/ Height2 cose oxidase peroxidase method.4 profile between cases and con-
(m). Serum cholesterol and Triglycer- trols.
5. Percent fat in body was cal- ide was measured using CHAD-
culated from BMI using the fol- PAP method (Boehringer Mann-
DISCUSSION
lowing formula: heim Ltd).5 HDL cholesterol was
Obesity, central distribution of
a. In males, % fat = 1.218 measured using well-established
fat, low level of physical activity
(Wt/ Ht2) - 10.13 precipitating properties of phos-
and high fat diet have close associ-
b. In females, % fat = 1.48 photungstic acid to precipitate
ation with Type 2 Diabetes Melli-
(Wt/ Ht2) -7.3 non HDL cholesterol.6 VLDL Cho-
tus.8 Now it is known that the adi-
6. Skin fold thickness was lesterol was measured by Fried-
pocyte specific hormone leptin,
measured using UNA skin fold wald's formula.7 LDL Cholesterol
the product of the obese (ob) gene,
caliper at four sites i.e. triceps, bi- was measured by the formula,
regulates adipose tissue mass
ceps, subscapular and suprailiac. LDL cholesterol = Total cholesterol
through hypothalamic effect on
- (HDL+VLDL).
satiety and energy expenditure.9
Table I: Comparison of obesity indices and plasma glucose between Obesity is associated with in-
Cases & Controls. creased plasma FFA levels that
Characteristics Case (n=60) Control (n=60) p value cause peripheral and hepatic insu-
lin resistance. Insulin resistance
Mean BMI(Kg/m2) 25.02±1.9 22.13±2.2 < .01
and FFA induced gluconeogene-
Mean SFT(mm) 44.02±3.9 42.23±2.2 < .01
sis stimulate insulin secretion. The
Mean Waist/hip ratio 0.79±0.8 0.70±0.04 < .01
result is no or minimal change in
% Fat 18.32±3.8 15.27±0.04 < .01
hepatic glucose production
Fasting Plasma Glucose (mg/dl) 127.16± 12.86 84.73±1.6 < .01
(HGP). However, in obese sub-
Post Prandial Glucose (mg/dl) 159.79±16.9 129.6±15.4 < .01
jects who are genetically predis-
posed to develop Type 2 Diabetes
Table II: Comparison of Lipid profile between Cases & Controls.
Mellitus, FFA fails to stimulate in-
Characteristics Case (n=60) Control (n=60) p value
sulin secretion. This, together
Mean serum Cholesterol (mg/dl) 225.6±40.5 172.9±25.5 < .01 with peripheral glucose underuti-
Mean serum triglyceride (mg/dl) 178.02±48.6 135.7±39.3 < .01 lization (attributable to uncom-
Mean serum VLDL (mg/dl) 37.81±16.9 27.13±3.28 < .01 pensated peripheral insulin re-
Mean serum LDL (mg/dl) 155.34±31.7 60.17±20.4 < .001 sistance), leads to increased I-IGP
Mean serum HDL (mg/dl) 50.82±4.7 70.1±1.2 < .01 that results in Type 2 Diabetes
International Journal of Health Information and Medical Research Vol: 1, Issue: 1, Jan 2014 13
Mellitus.10,11 Besides this, the bio-
logical process of aging leads to
loss in the ability to maintain glu-
cose homeostasis. Age-related de-
terioration in glucose tolerance
may be due to failing insulin secre-
tory capacity or insulin action, or
both.12
In Type 2 Diabetes Mellitus
subjects, increased levels of serum
cholesterol as compared to con-
trols (Table II) can be due to vari-
ous reasons.
1. Impaired, over stimulation
of HMG - COA reductase enzyme
by glucagon which is rate limiting
for cholesterol synthesis.
2. Defective catabolism of cho-
lesterol into bile acids also leads to
more cholesterol in blood.
3. More VLDL in plasma
causes hypercholesteremia be-
cause VLDL carries about 20% of
its total lipid content as choles-
terol.13
4. Cholesterol absorption in
Type 2 Diabetes Mellitus subjects
is significantly lower while choles-
terol synthesis significantly
higher. 14
Statistically very significantly
raised levels of serum triglyceride
and serum VLDL cholesterol were
found in Type 2 Diabetes Mellitus
as compared to controls (Table II).
NEFA (Non Esterified Fatty Ac-
ids) causes hepatic triglyceride
synthesis. The release of it as
VLDL is facilitated by insulin re-
sistance.15 This increased produc-
tion of VLDL is associated with
clearance defect, including lower
fractional catabolic rate for VLDL -
TG.
Lower adipose lipoprotein li-
pase (LPL) activity is dependent
upon insulin and is rate limiting
for triglyceride degradation.16 Se-
rum LDL Cholesterol is higher be-
cause VLDL is precursor of LDL
and raised VLDL may lead to in-
creased LDL levels associated
14 International Journal of Health Information and Medical Research Vol: 1, Issue: 1, Jan 2014
with decreased LDL catabolism.
LDL receptor is up regulated by
insulin but in Type 2 Diabetes
Mellitus due to insulin resistance,
there is less uptake of LDL.17
The decrease in HDL level is
statistically highly significant in
Type 2 Diabetes Mellitus subjects
when compared to controls
(p<0.01). This decrease may be due
to enhanced activity of LCAT (Ly-
solecithin Acyl Transferase) which
also causes hypertriglyceridemia.
In LDL rich cholesterol and phos-
pholipids, the enhanced LCAT ac-
tivity promotes the transfer of ac-
tivated fatty acids to cholesterol
resulting in formation of lysoleci-
thin, which in turn causes triglyc-
eride formation. This enhanced ac-
tivity impairs the formation of
HDL from LDL and hence HDL
Cholesterol is reduced signifi-
cantly in Type 2 Diabetes Melli-
tus.18
The findings in present study
are similar to various other studies
conducted in different parts of the
world.16, 19, 20, 21
CONCLUSION
The current study found that
obesity indices, cholesterol, Tri-
glyceride, VLDL, LDL were higher
and HDL levels were low in Type
2 Diabetes Mellitus, which may be
the cause for increased incidence
of coronary artery complications
in type 2 diabetes as corroborated
by studies conducted in different
parts of the world.
Conflict of Interest
None declared.
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