Pak J Physiol 2005;1(1-2)

GENDER DIFFERENCES IN LIPIDS AND LIPOPROTEIN (a) PROFILES

IN HEALTHY INDIVIDUALS AND PATIENTS WITH TYPE 2 DIABETES
MELLITUS
Syed Shahid Habib, Muhammad Aslam*, Waqas Hameed*
Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia and *Dept of Physiology, Army Medical
College, Rawalpindi

Background: This study aimed to assess gender differences in blood lipids and lipoprotein(a)
levels in healthy individuals and patients with type 2 diabetes mellitus. Methods: This study was
carried out at Department of Physiology, Army Medical College, Rawalpindi, Pakistan Sixty four
patients suffering from type 2 DM and forty one healthy individuals were studied. The subjects
were divided into healthy females, healthy males, type 2 DM females and type 2 DM males group.
Fasting blood samples were analyzed for lipoprotein(a) [Lp(a)], total cholesterol (TC),
triglycerides (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein
cholesterol (HDL-C), glucose and glycosylated hemoglobin (HbA1c). Results: When the lipid
profile of healthy females was compared with the lipid profile of healthy males it was observed
that HDL-C levels were significantly higher in healthy females as compared to healthy males (p <
0.05) while serum triglycerides were significantly raised in healthy males as compared to healthy
females(p < 0.05). Diabetic females had significantly higher levels of LDL-C, HDL-C , TG and
Lp(a) levels as compared to healthy females (p < 0.01, p < 0.05, p < 0.05 and p < 0.05). Diabetic
males had significantly higher levels of TC, LDL-C, HDL-C and Lp(a) levels than healthy males
(p < 0.01, p < 0.05, p < 0.01, and p < 0.05). The difference in lipid and Lp(a) profile was non
significant between diabetic females and diabetic males. Conclusions: There are gender
differences in lipid profile in patients with type 2 diabetes mellitus and well as healthy individuals.
Diabetic individuals have raised levels of Lp(a) as compared to non diabetic subjects in case of
both females and males. However in diabetic females and diabetic males there is no difference in
lipid profile and Lp(a) concentrations. Further studies are needed to confirm these findings.
Key Words : Type 2 Diabetes Mellitus, Lipids, Lipoproteins, Lipoprotein (a) Glycosylated
Hemoglobin.

INTRODUCTION or HRT. Being overweight or obese during the

menopausal transition is not necessarily associated
Heart disease is the number one cause of death in with deterioration in coronary risk factors.3
women, as it is in men; risk factors include high Cardiovascular disease, may pose greater risk for
cholesterol, high triglycerides, low HDL-C, diabetes, women than for men. For example, the risk factors,
hypertension, gender and cigarette smoking. The testing modalities, presenting symptoms and the
lipoprotein profile of a woman undergoes many therapeutic choices made for women with coronary
changes during her lifetime because of the effects of artery disease are significantly different from those
endogenous hormones at pregnancy, the for men. Low levels of high-density lipoprotein
administration of oral contraceptives, and estrogen cholesterol (HDL-C), <35 mg/dL in men and <45
replacement at the menopause. Endogenous estrogen mg/dL in women, is associated with a greater risk of
reduces the risk of heart disease in women as does coronary artery disease and more progression of
unopposed estrogen replacement in the menopause. angiographically demo nstrated disease in women,
An increase in the incidence of coronary heart while increasing HDL-C has a more cardioprotective
disease risk has commonly been reported in effect in the female than in the male population. The
postmenopausal women.1 total cholesterol-to-HDL-C ratio is also more
The incidence of coronary heart disease (CHD) is predictive of coronary artery disease in women than
much lower in younger women than in age-matched in men. Diabetes is particularly hazardous in women,
men, and this has led to the popular misconception and low HDL-C levels constitute a disproportionate
that cardiovascular disease is a disease of men, and is risk for coronary artery disease in diabetic women
relatively rare in women. The incidence of CHD may compared with diabetic men.4 Very high prevalence
be much lower in young women than in men of the of dyslipidemia has been reported in healthy
same age, up to the age of 65. However after the age postmenopausal women.5
65, the risk equalizes for both sexes.2 The misconception that women are at low risk of
During the perimenopausal period there is a weight CHD has been influenced by many large studies of
gain that does not seem to depend on the menopause
 Pak J Physiol 2005;1(1-2)

cardiovascular disease in which women are under- infections, diabetic ketoacidosis and non ketotic
represented, with the majority of trials being hyperosmolar diabetes. The patients having any of
conducted in White, middle-aged men.6-8 In addition the above mentioned disorders were excluded from
to, or as a result of, the treatment bias, women with the study. Those patients giving history of familial
CHD also have a worse outcome than men. The hypercholesterolemias, ischaemic heart disease or
precise reasons for the poorer outcomes are difficult myocardial infarction were also excluded from the
to ascertain, but women tend to present at an older study. The history of medication was recorded and
age and have more complicating factors such as the patients taking lipid lowering agents, oral
diabetes, hypertension and heart failure than men.9,10 contraceptives, hormone replacement therapy and
Most of the research on cholesterol and steroids were also excluded.
cardiovascular risk has been performed on men and Blood pressure (SBP/DBP) was recorded in sitting
the data extrapolated to women.2 This approach has position in the right arm in mmHg. The subjects
been questioned, since it is well-established that included in the healthy group were age, sex and BMI
oestrogen affects lipid metabolism.11,12 Lipoprotein matched healthy individuals. They were not suffering
levels strongly predict incident and recurrent CAD from any acute infection or any metabolic or
events in both sexes, and LDL particle size may be a psychological disorder. They had no family history of
better predictor of premature CAD in women than of hypercholesterolemias or DM. Their lipid profile and
CAD associated with advanced age. The effects of fasting blood glucose were estimated. They had
postmenopausal hormonal therapy on lipoprotein normal lipid profile and fasting blood glucose level
levels are complex, and the benefits of such therapy less than 6.1 mmol/l (110 mg/dl).
are not established. In contrast, lifestyle changes and Glucose was estimated by GOD–PAP (Glucose
pharmacological lipid-lowering therapy have been Oxidase Phenyl Ampyrone) method, an enzymatic
shown to favorably influence the natural course of colorimetric method with the kit supplied by Linear
atherosclerotic disease and reduce cardiovascular Chemicals (Cat No.GL-5083). Total Cholesterol was
events in men and women.13 Studies are needed to measured by CHOD-PAP (Cholesterol Oxidase
explore the differences in dyslipidemia of females Phenol Ampyrone), an enzymatic colorimetric
and males. Moreover age related changes also need to method, using kits of Linear Chemicals, Spain (Cat
be explored. No. CH 5054). GPO-PAP (Glycerol Phosphate
Therefore we aimed to study gender based Oxidase), an enzymatic colorimetric method was
differences in lipid and Lp(a) profile in non diabetic used for serum triglycerides estimation. The kit was
healthy individuals and patients with type 2 DM. supplied by Linear chemicals (Cat No TR 5046). The
instrument used was Selectra 2 autoanalyzer. CHOD
PATIENTS AND METHODS – PAP Method was used for HDL-C and LDL-C
This study was carried out at Army Medical College estimation with the kit was supplied by Merck
and Armed Forces Institute of Pathology (AFIP), Systems (Cat No; 28248). Ion exchange resin
Rawalpindi. Sixty four patients suffering from type 2 separation method was used for estimation of
DM and forty one healthy individuals were studied. Glycosylated Haemoglobin. The kit was supplied by
The subjects were divided into four groups. Stanbio Glycohemoglobin [Pre-Fil]. Serum Lp(a)
Group A consisted of healthy female subjects levels were measured immunochemically with a
Group B consisted of healthy male subjects Sandwich ELISA that uses a mouse monoclonal anti-
Group C consisted of type 2 DM female subjects apo(a) antibody as the solid phase antibody and a
Group D consisted of type 2 DM male subjects sheep antiapo B-100 polyclonal antibody (antibody
All patients were diagnosed cases of type 2 DM. against B-100) as the detection antibody. The
Patients were selected on the basis that there were antibodies used in this assay identify all known
non significant differences in their clinical isoforms of apo(a). There was no cross-reactivity
characteristics and glycaemic status. Thirty four with plasminogen and LDL. The kits used were
patients were males and twenty six were females. supplied by Innogenetics Biotechnology for Health
Their height was measured in centimeters and weight Care, Gent, Belgium.
in kilograms. Body mass index (BMI) was calculated The data was analyzed by SPSS (version 10,
by the following formula; Chicago). Data was expressed as mean and standard
BMI = Body Weight in Kilograms / Height (square meters) error of mean (SEM). The tests applied for statistical
All the patients were in stable metabolic condition. analysis were one way analysis of variance
History was taken regarding any disease that could (ANOVA) and Bonferroni (Multiple comparisons)
affect the metabolic status of the body and the for comparison differences between studied groups. p
parameters studied like nephrotic syndrome, acute or value = 0.05 was taken as significant.
chronic renal failure, thyroid disorders, acute
 Pak J Physiol 2005;1(1-2)

RESULTS LDL-C, HDL-C and Lp(a) levels in diabetic males (p

< 0.01, p < 0.05, p < 0.01, and p < 0.05 respectively).
Both healthy subjects and DM patients were divided In case of diabetic females and diabetic males the
into male and female groups and their clinical difference in lipid and Lp(a) profile was non
characteristics were compared. There were non significant.
significant differences in the clinical characteristics
among different groups. All subject were matched for DISCUSSION
age and BMI. Both SBP and DBP were significantly
Women have significantly different lipid, apoprotein,
higher in diabetic females as compared to healthy
and lipoprotein profiles than men.regardless of
females (p< 0.0001 and p < 0.05 respectively). Also
menopausal status. In a population sample of women
in males both SBP and DBP were significantly higher
there were lower values of BMI, TG, TC/HDL ratio
in diabetics as compared to healthy subjects (p<
and higher levels of HDL-C than men.14 Gender
0.0001 and p < 0.001 respectively). There was no
affects lipid parameters and this effect is independent
difference in SBP or DBP between males and
of age and menopausal status.15 Presumably these
females in case of both healthy individuals as well as
differences are due to the different levels of
diabetics.
circulating sex hormones, specifically estrogens and
When the lipid profile of healthy females was
androgens in women versus men. It has been reported
compared with the lipid profile of healthy males it
that women have higher production rates of apoA-I,
was observed that there was a significant difference
the major HDL apoprotein, than do men, and that
in serum HDL-C and serum triglyceride levels while
levels of apoA-I and production rates of apoA-I and
there was no difference in TC, LDL-C and Lp(a)
Lp A-I can be increased with estrogen
levels. HDL-C levels were significantly lower in
administration.16
healthy females as compared to heathy males (p <
For screening purposes, one measurement of serum
0.05) while serum triglycerides were significantly
total cholesterol in a woman gives a good estimate of
raised in healthy males as compared to healthy
the long-term level. The current data indicate that
females(p < 0.05).
repeated measurements of serum total cholesterol do
When heaithy females were compared with diabetic
not improve the predictability of future cholesterol
females we observed significantly higher levels of
levels. The data also suggest that, at least in
LDL-C, HDL-C , TG and Lp(a) levels in diabetic
postmenopausal women with an elevated level of
females (p < 0.01, p < 0.05, p < 0.05 and p < 0.05
serum total cholesterol, one should proceed
respectively).
immediately to lipoprotein analysis for further risk
When heaithy males were compared with diabetic
assessment.17
males we observed significantly higher levels of TC,
Table-1: Clinical characteristics, Glycaemic status and insulin levels in healthy and diabetic subjects (Data is
expressed as Mean ± SEM).
Healthy Females Healthy Males Diabetic Females Diabetic Males
N=25 N=16 N=29 N=35
Age (years) 47.36 ± 1.14 46.62 ± 1.78 47.17 ± 1.72 48.24 ± 2.30
BMI ( kg/ m2 ) 25.81 ± 0.65 24.96 ± 0.44 26.36 ± 0.99 25.32 ±.70
SBP (mmHg) 129.60 ± 2.56 125.31 ± 2.06 144.13 ± 2.45 ### 143.62 ± 2.96 ¶¶¶
DBP (mmHg) 79.60 ± 1.62 78.75 ± 1.67 85.34 ± 1.70 # 88.10 ± 1.72 ¶
FG (mmol/l) 5.02 ± 0.14 5.08 0 ± 0.12 10.75 ± 0.45 9.08 ± 0.65
HbA1c % 4.74 ± 0.08 4.82 ± 0.10 7.35 ± 0.24 6.95 ± 0.27
# p< 0.05 compared to healthy females # # # p< 0.0001 compared to healthy females
¶ p< 0.05 compared to healthy males ¶¶ ¶p< 0.0001 compared to healthy male

Table-2: Fasting lipid and Lp(a) profile in healthy and diabetic subjects (Data is expressed as Mean ± SEM)
Healthy Females Healthy Males Diabetic Females Diabetic Males
N=25 N=16 N=29 N=35
T Chol (mmol/l) 4.28 ± 0.13 4.32 ± 0.18 4.65 ± 0.18 4.97 ± 0.19 ¶¶
LDL-C (mmol/l) 2.61 ± 0.12 2.59 ± 0.17 3.03 ± 0.13 ## 3.10 ± 0.19 ¶
HDL-C (mmol/l) 1.20 ± 0.02 1.08 ± 0.04* 0.95 ± 0.04 # 1.02 ± 0.04 ¶¶
TG (mmol/l) 1.12 ± 0.10 1.46 ± 0.009* 2.05 ± 0.30 # 1.69 ± 0.12
Lp(a) [mg/dl] 20.82 ± 5.3 18.34 ± 4.3 47.58 ± 7.60 # 54.67 ±10.19 ¶
* p< 0.05 compared to healthy females # p< 0.05 compared to healthy females,
# # p< 0.01 compared to healthy females ¶ p< 0.05 compared to healthy males
¶¶ p< 0.01 compared to healthy males
 Pak J Physiol 2005;1(1-2)

contrast, elderly women have higher total cholesterol

Increased rates of coronary heart disease (CHD) and younger men have lower HDL-cholesterol.21 In a
occur with advancing age in both sexes, although cross-sectional study, Weiss et al22 found that
CHD rates in women lag behind those of men by postmenopausal women had significantly higher
about 10 years. There is a sharp increase in CHD rate serum cholesterol compared to pre-menopausal
among women after approximately 50 years of age. women. In the Framingham Study23 women between
The reasons for this are not completely understood the ages of 29 and 62 years who were followed-up in
and are undoubtedly multifactorial. Cross-sectional a longitudinal study for 18 years demonstrated a
data from large-scale population studies suggest that significant rise in serum cholesterol levels between
around the time of the menopause, low-density premenopausal and postmenopausal examinations,
lipoprotein (LDL)-cholesterol levels increase by with the rise taking place within a short time of the
approximately 15 to 25%. Because this increase is onset of the menopause, thus suggesting a causal
larger than that observed in men over the same age effect.
span and closely approximates that observed in Nevertheless, not all studies have confirmed this
women after oophorectomy, it is likely that reduced relationship. For example, in a study of Pima Indian
circulating estrogen levels associated with women, no association was found between the
menopause play a role in the adverse changes in both menopause and serum cholesterol levels.24 It has been
blood lipid levels and CHD incidence. There is clear suggested that this is due to the diet of Pima Indians,
evidence that treating hypercholesterolemia reduces which is generally lower in cholesterol than that of
cardiovascular risk in women, as well as in men. The Whites and thus, environmental factors may play an
favourable effects of statins on high-density additional and important role in the increase in
lipoprotein (HDL)-cholesterol and triglyceride levels cholesterol seen in older White women.
are more modest, and statins are not known to Lipoprotein (a) is a lipoprotein which has been
decrease lipoprotein (a) [Lp(a)] levels. Estrogen or related to thrombogenesis and atherogenesis. Clinical
hormone replacement therapy (ERT/HRT) and data, mainly from cross-sectional studies, have shown
nicotinic acid improve LDL- and HDL-cholesterol that this molecule can be positively associated with
levels and also decrease Lp(a) levels. Treatment an increased risk of CHD and stroke.25 In a study by
should be individualised for each patient. It is Lip et al26 plasma levels of lipoprotein (a) were
important to evaluate the primary form of significantly increased compared to base-line,
dyslipidaemia, other CHD risk factors, comorbidities, following hysterectomy and bilateral oophorectomy.
and the extent of lipid improvement needed in order In the Framingham Offspring study,27 however, no
to reach treatment goals.18 significant association was found between the
Hypertension is one of the major risk factors for the menopause and lipoprotein(a) levels. Lipoprotein(a)
development of CHD. The incidence of hypertension is an independent risk factor for CHD and there is
increases with age and is higher in men than in some evidence that lipoprotein (a) increases with age
women up to the age of about 50. Beyond middle age, in women.28 Another study has shown that Lp(a) was
however, blood pressure in women exceeds that in a significant risk factor for CAD in both pre- and
men. It has been suggested that menopause may postmenopausal women.29 Lp(a) measurement is of
potentiate the age-related increase in systolic value in investigation of patients at risk for CAD and
pressure, perhaps as a result of reduced arterial that it is a particularly useful predictor of risk in
compliance. Staessen et al19 measured the blood women.30
pressures of 315 women and followed them up for a Diabetes increases the risk of CHD threefold in
median of 5.2 years. Those women who were post- women, and puts them at the same risk of CHD as
menopausal had a 4–5 mmHg higher systolic blood men of the same age. Much of this excess risk is due
pressure than their pre- and perimenopausal to the excess in other coronary risk factors which
counterparts, and also, while there was no change in occur in diabetics.31
systolic blood pressure in premenopausal women In the Nurses’ Health Study32 body mass index was
during follow-up, the systolic blood pressure strongly associated with death due to CHD, with the
increased by 4 mmHg in 5 years in the risk of CHD over three times higher among women
postmenopausal and perimenopausal women. with a body mass index of 29 or higher. Much of this
Large epidemiological studies have found a sex increased risk can be attributed to influences on blood
difference in lipoprotein distribution. These pressure, glucose tolerance and lipid levels. However,
differences may in part explain the difference in the the presence of diabetes seems to negate any
incidence of CHD between the sexes. Younger cardioprotection that a woman may have. The
women, however, have lower LDL- cholesterol and findings of the present study are in line with these
higher HDL-cholesterol compared to men.20 In findings.
 Pak J Physiol 2005;1(1-2)

Conclusions plasma lipoprotein metabolism in premenopausal females, J.

Clin. Endocrinol. Metab. 1983; 57: 262-270.
There are gender differences in lipid profile in 17. Hetland ML, Haarbo J, Christiansen C.One measurement of
serum total cholesterol is enough to predict future levels in
patients with type 2 diabetes mellitus and well as healthy postmenopausal women. Am J Med 1992
healthy individuals. Diabetic individuals have raised Jan;92(1):25-8
levels of Lp(a) as compared to non diabetic subjects 18. Davidson MH, Maki KC, Karp SK, Ingram KA.Management
in case of both females and males. However in of hypercholesterolaemia in postmenopausal women. Drugs
Aging 2002;19(3):169-78
diabetic females and diabetic males there is no 19. Staessen JA, Ginocchio G, Thijs L, Fagard R. Conventional
difference in lipid profile and Lp(a) concentrations. and ambulatory blood pressure and menopause in a
Further studies are needed to confirm these findings. prospective population study. J Human Hypertens 1997;
11:507–14.
REFERENCES 20. Barr DR, Russ EM, Eder HA. Protein-lipid relationships in
human plasma. Am J Med 1951; 11:480–93.
1. Miller VT. Dyslipoproteinemia in women. Special 21.
Nikkila M, Pitkajarvi T, Koivula T, Lehtomaki E, Jokela H.
considerat ions. Endocrinol Metab Clin North Am 1990 Age-related changes and sex differences in serum lipid
Jun;19(2):381-98 concentrations in health-screening subjects. Cardiovasc Risk
2. E. Edmunds,G.Y.H. Lip. Cardiovascular risk in women: the Factors 1991; 1:204–10.
cardiologist's perspective Q J Med 2000; 93: 135-145 22.
Weiss NS. Relationship of menopause to serum cholesterol
3. Bulliyya G. Risk of coronary heart disease in women after and arterial blood pressure: the United States’ Health
menopause. J Indian Med Assoc 2001 Sep;99(9):478-80, Examination Survey of adults. Am J Epidemiol 1972;
482. 96:237–41.
4. Blumel JE, Castelo-Branco C, Rocangliolo ME, Bifa L, 23.
Hjortland MC, McNamara PM, Kannel WB. Some
Tacla X, Mamani L. Changes in body mass index around atherogenic concomitants of menopause: the Framingham
menopause: a population study of Chilean woman. Study. Am J Epidemiol 1976; 103:304–11.
Menopause 2001 Jul-Aug;8(4):239-44. 24.
Hamman RF, Bennett PH, Miller M. The effect of
5. Legato MJ. Dyslipidemia, gender, and the role of high- menopause on serum cholesterol in American Pima Indian
density lipoprotein cholesterol: implications for therapy. Am women. Am J Epidemiol 1975; 102:164–9.
J Cardiol 2000 Dec 21;86(12A):15L-18L 25.
Lip GYH, Jones AF. Lipoprotein (a) and vascular disease:
6. Khaw KT. Where are the women in studies of coronary heart thrombogenesis and atherogenesis. Q J Med 1995; 88:529–
disease? Br Med J 1993; 306:1145–6. 39.
7. Wenger NK. Exclusion of the elderly and women from 26.
Lip GYH, Blann AD, Jones AF, Beevers DG. Effects of
coronary trials. Is their quality of care compromised? JAMA hormone-replacement therapy on hemostatic factors, lipid
1992; 268:1460–1. factors, and endothelial function in women undergoing
8. Wenger NK. Cardiovascular drugs: the urgent need for surgical menopause: Implications for prevention of
studies in women. J Am Med Womens Assoc 1991; 46:117– atherosclerosis. Am Heart J 1997; 134:764–71.
20. 27.
Jenner JL, Ordovas JM, Lamon-Fava S, Schaefer MM,
9. Dittrich H, Gilpin E, Nicod P, Cali G, Henning H, Ross J. Wilson P, Castelli WP, Schaefer EJ. Effects of age, sex, and
Acute myocardial infarction in women: influences of gender menopausal status on plasma lipoprotein(a) levels: the
on mortality and prognostic variables. Am J Cardiol 1988; Framingham Offspring Study. Circulation 1993; 87:1135–41.
62:1–7. 28.
Sandkamp M, Assman G. Lipoprotein (a) in PROCAM
10. Fiebach NH, Viscoli CM, Horwitz RI. Differences between participants and young myocardial infarction survivors. In:
women and men in survival after myocardial infarction: Scanv AM, ed. Lipoprotein(a): 25 years of progress. New
biology or methodology? JAMA 1990; 263:1092–6. York, Academic Press, 1990:205–9.
11. Barr DR, Russ EM, Eder HA. Protein-lipid relationships in 29.
Orth-gomer k, Mittleman MA, Schenck-gustafsson K,
human plasma. Am J Med 1951; 11:480–93. Wamala SP, Eriksson M, Belkie K, Kirkeeide R, Svane B,
12. Barr DR, Russ EM, Eder HA. Influence of oestrogen on RydenL. Lipoprotein(a) as a determinant of coronary heart
lipoproteins in atherosclerosis. Trans Assoc Am Phys 1952; disease in young women. Circulation 1997;95: 329-334,.
65:102–11. 30.
Frohlich J, Dobiasova M, Adler L, Francis M. Gender
13. Bittner V.Lipoprotein abnormalities related to women's differences in plasma levels of lipoprotein (a) in patients with
health. Am J Cardiol 2002 Oct 17;90(8A):77i- 84i angiographically proven coronary artery disease.
14. Li Z, McNamara JR, Fruchart JC, Luc G, Bard JM, Ordovas Physiol Res. 2004;53(5):481-6.
JM, Wilson PW, Schaefer EJ.Effects of gender and 31.
Kannel WB. Metabolic risk factors for coronary heart disease
menopausal status on plasma lipoprotein subspecies and in women; Perspective from the Framingham Study. Am
particle sizes. J Lipid Res. 1996 Sep;37(9):1886-96. Heart J 1987; 114:413–19.
15. Tremollieres FA, Pouilles JM, Cauneille C, Ribot C. 32.
Manson JE, Willett WC, Stampfer MJ, Colditz GA, Hunter
Coronary heart disease risk factors and menopause: a study in DJ, Hankinson SE, Hennekens CH, Speizer FE. Body weight
1684 French women. Atherosclerosis 1999 Feb;142(2):415- and mortality among women. N Engl J Med 1995; 333:677–
23. 85
16. Schaefer, E. J., D. A. Foster, L. A. Zech, H. B. Brewer, Jr.,
and R. I. Levy.. The effect of estrogen administration on
_____________________________________________________________________________________________________________________
Address For Correspondence:
Dr Syed Shahid Habib, Department of Physiology (29), College of Medicine, P.O. Box 2925, King Saud
University, Riyadh 11461, Kingdom of Saudi Arabia.
Email: shahidhabib44@hotmail.com