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Journal of the American College of Nutrition, Vol. 26, No. 3, 250-258 (2007)
Published by the American College of Nutrition

An Investigation of Hormone and Lipid Associations after Weight Loss in Women

Sylvia Santosa, PhD, Isabelle Demonty, PhD, Alice H. Lichtenstein, DSc, Katherine Cianflone, PhD and Peter J.H. Jones, PhD

School of Dietetics and Human Nutrition, McGill University, Ste-Anne-de-Bellevue
McGill University Health Center, Division of Cardiology, Montreal, Quebec, CANADA
Jean Mayer USDA HNRCA at Tufts University, Boston, Massachusetts

Address reprint requests to: Peter JH Jones, PhD, Richardson Centre for Functional Foods and Nutraceuticals, University of Manitoba, Smartpark, 196 Innovation Drive, Winnipeg, Manitoba, R3T 6C5, CANADA. E-mail: peter_jones{at}umanitoba.ca


   ABSTRACT
TOP
 FOOTNOTES
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Objective: The objectives of this study were to determine 1) whether the extent of weight loss is predictive of the degree of changes in hormone and lipid levels; 2) the interactions between energy regulating hormones after weight loss through an energy deficit/exercise protocol diet and exercise; 3) whether initial metabolic parameters are indicative of the extent of weight loss.

Methods: Thirty-five hyperlipidemic females (BMI 28–39 kg/m2) 35–60 years old participated in a six month weight loss trial. Weight loss resulted from a diet and exercise program that when combined produced a 30% energy deficit. Fasting plasma taken during 2 wk stabilization periods at the beginning and end of the study was analysed for lipids, hormone and glucose levels.

Results: Average weight loss was 11.7 ± 2.5 kg (p < 0.0001). TC, LDL-C, and triacylglycerols decreased 9.3 ± 9.5% (p < 0.0001), 7.4 ± 12.2% (p < 0.001), and 26.8 ± 19.6% (p < 0.05), respectively, while HDL-C increased (p < 0.05) by 8.2 ± 16.3%. Leptin levels declined (p < 0.001) 48.9 ± 16.0% and ghrelin levels rose (p < 0.001) 21.2 ± 26.7%. While overall levels of adiponectin did not differ, individual values changed such that weight loss predicted increases in adiponectin levels. Though initial weight did not predict weight loss, baseline lipid and insulin levels positively predicted weight loss.

Conclusion: Initial metabolic parameters may be predictors of weight loss. Beneficial effects of weight loss as achieved through diet and exercise on measured parameters indicate moderate weight loss reduces key risk factors of cardiovascular disease in overweight individuals.

Key words: weight loss, women, cholesterol, adipocyte hormones, ghrelin


   INTRODUCTION
TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The most recent revisions of dietary guidelines by the American Heart Association emphasize the importance of weight management to decrease CVD risk [1]. Similarly, weight management is emphasized by the American Diabetes Association [2]. Since CVD and diabetes are primary consequences of obesity and major causes of death and disability in the Western world, it is important to understand the role of weight loss on management and prevention of these diseases.

One of the main reasons that overweight individuals are at increased risk of developing CVD is due to the dyslipidemia that often accompanies this condition. Many trials have been conducted that examine the effects of weight loss on plasma lipid concentrations [3,4]. However, few studies have combined moderate energy expenditure and intake reduction in a highly controlled manner in females. Additionally, the relationship between extent of change in weight versus lipid levels has not been fully elucidated.

Ghrelin, adiponectin, and leptin are three hormones that are likely affected by weight loss. Adiponectin and leptin are adipocytokines, while ghrelin is predominantly released from stomach. Ghrelin and leptin affect energy homeostasis through opposing effects. Leptin decreases feeding by signalling satiety and stimulating energy expenditure, while ghrelin stimulates food intake and energy storage [5,6]. Studies have shown that leptin is often elevated in people with higher body fat, as is found in obesity [5,7]. In contrast, adiponectin levels have been shown to be reduced in obese subjects [8]. Adiponectin is also attenuated in patients with insulin-resistance and type 2 diabetes and thus, may have some function in regulation of blood glucose homeostasis [9,10]. Levels of adiponectin have also been shown to be lower in those with CVD [11,12]. However, whether changes in adiponectin reduce risk of CVD and type 2 diabetes is uncertain. Despite the implications of ghrelin, adiponectin, and leptin in weight loss, no studies yet exist that examine changes in these hormones combined in the context of weight loss through diet and exercise.

Previous research has shown that initial metabolic status may influence extent of weight loss. However, studies examined have only accounted for the effect of initial insulin levels and weight [13,14]. Baseline levels of other hormones, specifically leptin, adiponectin, and ghrelin, that regulate appetite may affect ability to lose weight. Thus, determining the extent to which baseline metabolic characteristics result in successful weight loss may help in deciding the most effective course of treatment of overweight individuals.

The present study uses energy restriction to investigate the potential effects and associations between lipid and hormone parameters, which have not previously been examined in combination after moderate weight loss. Though these parameters have been studied individually after weight loss in men, few studies examine women. In this study, only women were included to investigate the potential of weight loss to affect hormone and lipid risk factors of CVD and type 2 diabetes in this population. Additionally, the novel incorporation of pre and post periods of stabilization will minimize variation and enhance the isolation of the effect of weight loss. In this study, we hypothesized that significant weight loss in overweight and obese hyperlipidemic women results in favourable changes to blood lipid profiles, glucose, insulin, and adiponectin, while decreasing levels of leptin and increasing levels of ghrelin. It is also hypothesized that changes in body weight will be reflected in the degree of changes in the measured parameters. Furthermore, we hypothesized that baseline weight and initial levels of blood lipid, c-reactive protein (CRP), insulin, glucose, adiponectin, leptin, and ghrelin would be predictive of weight loss.


   MATERIALS AND METHODS
TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects
Hyperlipidemic, but otherwise healthy, free-living overweight and obese female volunteers were recruited. The subjects, aged between 35 and 58 y, had initial body mass indices of 28–39 kg/m2. Premenopausal and postmenopausal subjects were included, as well as those who were perimenopausal provided they were either not taking or on stable hormone replacement therapy (HRT) for at least 6 months prior to the commencement of the study. Subjects were screened for circulating LDL-C and TAG concentrations. Inclusion criteria included fasting plasma LDL-C concentrations of 3.4–6.7 mmol/L and TAG concentrations >1.5 mmol/L. Use of oral anti-hypertensive agents and thyroid hormones were permitted, provided they were stable and continued throughout the duration of the study. Before acceptance, subjects were required to provide a medical history and to undergo a complete physical examination. Fasting blood samples were collected for serum biochemistry and hematology. Subjects were screened for chronic illness, including hepatic, renal, gastrointestinal, and cardiac dysfunction, before admission into the study. Additionally, those who were found to have previous history of eating disorders, chronic laxative use, or excessive exercise were excluded. Those undergoing oral hyperlipidemic therapy less than six months prior to commencement of the study were also excluded. Before the start of the study, subjects received the study protocol and discussed any queries with the primary investigator or the study co-ordinators before signing the consent form. The experimental protocol was approved by the Faculty of Medicine Ethics Review Board at McGill University, Montreal, QC, Canada and the Human Investigation Review Committee of Tufts University, Boston, MA, USA.

Experimental Design
Subjects served as their own controls in a longitudinal before and after study design. Overall, the trial consisted of three dietary periods; pre-loss stabilization, weight loss and post-loss stabilization periods.

The first and third dietary periods were identical, with each lasting two weeks in duration. During these periods subjects were required to maintain a stable weight, as well as, usual food and exercise habits. To ensure weight maintenance during the stabilization periods, subjects were weighed at days 1, 5, 8, 12, and 15 during period 1 and days 155, 159, 162, 166, and 169 during period 3. Compliance during the stabilization period was defined as average weight during the stabilization periods ± 1 kg. Data are reported for days 15 and 169.

Following the initial two week stabilization period, subjects underwent the 20 week weight loss period, during which, they were counselled to decrease energy intake by 20% and increase energy expenditure by 10%. To achieve the 20% decrease in energy consumption, each subject was provided with individual dietary instruction at the start and for the duration of the weight loss period. Diets were formatted for each volunteer using an exchange system that provided 50–60% of energy from carbohydrates, 20% of energy from protein and <30% of energy from fat. Subjects also received pamphlets containing basic nutrition information, as well as, sample recipes and menus to aid them in the application of dietary principles.

To achieve a 10% increase in energy expenditure, subjects worked with a personal trainer who demonstrated and taught proper exercise techniques, and assigned exercise routines. Subjects were given the option to perform exercise independently, or within the gym facility at the Mary Emily Clinical Nutrition Research Unit at McGill University.

Compliance to the protocol was monitored by weight loss at weekly weigh-ins. Additionally, participants were encouraged through the use of an award point system and visual graphs on which they were able to plot weight loss.

Fasting blood samples were taken at day 1, 8, and 15 during the first stabilization period and at day 155, 162, and 169 during the second stabilization period for measurement of circulating lipid concentrations. Baseline and endpoint lipid measurements, as well as apolipoproteins (apo) A1 and B100 concentrations, were analysed at days 15 and 169. Glucose, insulin, adiponectin, and leptin and ghrelin were measured at days 14, 15, 168 and 169. Days 14 and 15, and days 168 and 169 were then averaged to reduce day-to-day variation.

Plasma Analyses
Fasting plasma was separated from red blood cells (RBC) by centrifugation at 20°C for 15 min at 520 x g within 30 minutes of phlebotomy. Samples were then stored at –20°C until analysis. Plasma TC, HDL-C, and TAG concentrations were analysed in duplicate by automated methods through a Hitachi 911 automated analyzer (Roche Diagnostics, Indianapolis, IN) using enzymatic or immunoturbidometric reagents [15]. LDL-C was determined directly by the dextran/magnesium sulfate method in order to separate it from HDL-C (N-geneous LDL C assay, Equal Diagnostics) [16,17]. Apo A1 and B100 were measured using an Abbott Spectrum CCX Analyzer (Abbott Laboratories, Dallas, TX) using reagents and calibrators from INCSTAR (Stillwater, MN). Immunoprecipitates of antibody-apoprotein complexes were quantified by turbidimetry [18,19]. The assays are standardized through the Lipid Standardization Program of the Centers for Disease Control (Atlanta, GA). C-reactive protein (CRP) was measured using a Tina-quant CRP (Latex) High Sensitive immunoturbidimetric assay (Roche Diagnostics). In brief, anti-CRP antibodies coupled to latex microparticles react with CRP to form a complex which is measured turbidimetrically using a Hitachi 911 automated analyzer (Roche Diagnostics). Glucose was analysed by enzymatic method using the glucose (trinder) reagent from Sigma Diagnostics (St Louis, MO, USA). Concentrations of insulin, adiponectin, leptin, and ghrelin were determined by the RIA method using kits from Linco Research Inc. (St. Charles, MO) [20].

Statistics
All data are expressed as means ± SDs. The statistical significance of changes in body weight, and lipoprotein cholesterol, TAG, apo A1, apo B100, and CRP was determined using a Student's paired t-tests on values obtained after the two stabilization periods on days 15 and 169. Log transformations were conducted on apo A1 and apo B100 before applying Student's paired t-tests. A Wilcoxon signed rank test was used to compare changes in CRP. Days 14 and 15 and days 168 and 169 were first averaged for glucose, insulin, leptin, adiponectin, and ghrelin concentrations before a Student's paired t-test was carried out on their averages. Log transformations were conducted on leptin and adiponectin before applying Student's paired t-tests. Stability of plasma lipid cholesterol concentrations during the stabilization periods was verified using repeated measures analysis of variance (ANOVA). Linear regression analysis was used to determine the relationship between weight loss and changes in lipid, CRP, glucose, and hormone measures. Forward stepwise regression and best subset analyses were used to determine the predictive values of baseline weight and initial biochemical parameters to weight loss. Pearson correlations were used to determine the relationship between lipid parameters, glucose, insulin, leptin, adiponectin, and ghrelin. All values were defined to be statistically significant at p < 0.05. Data were analysed using SPSS for Windows (version 12.0.0; SPSS Inc., Chicago, IL).


   RESULTS
TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Forty-two subjects were enrolled in the study. Two dropped out at the beginning of the study due to inability to fulfill study requirements and five dropped out because they had difficulty adhering to the weight loss regime and could not adhere to the study visit schedules. Therefore, complete data were collected for 35 participants and analysed as per the study protocol. The average age of the subjects who completed the study was 49.4 ± 6.7 years. Individual weight loss throughout the study is shown in Fig. 1. Overall, participants lost an average of 11.7 ± 2.5 kg (14.5 ± 3.1% of original body weight) (p < 0.001).


Figure 1
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  		Fig. 1. Weekly changes in weight of individual participants throughout the study. Line shown is based on regression lines of each study period. Formulas for the regression lines are y = –0.01x + 0.22; r2 = 0.016, p > 0.05 for the pre weight loss stabilization period (days 1–15), y = –0.10x + 0.76; r2 = 0.997, p < 0.001 for the weight loss period (days 0–155), and y = 0.02x – 17.43; r2 = 0.167, p < 0.02 for the post weight loss stabilization period.

 
Changes in Biochemical Parameters in Response to Weight Loss
No significant differences in lipoprotein cholesterol were found between days 1, 8, and 15, and between days 155, 162, and 169 of the stabilization periods (data not shown). Average circulating plasma lipoprotein cholesterol, TAG, apo A1, apo B100, CRP, glucose, insulin, leptin, adiponectin, and ghrelin levels before and after the study period, as well as, mean changes after weight loss are shown in Table 1. Both TC and LDL-C levels decreased (p < 0.001) 0.62 ± 0.65 mmol/L, and 0.32 ± 0.51 mmol/L (p = 0.001), respectively. Weight loss also resulted in a reduction (p < 0.001) of TAG levels by 0.55 ± 0.46 mmol/L and an increase (p = 0.03) in HDL-C levels by 0.08 ± 0.21 mmol/L. Additionally, there was a decline (p = 0.001 and p < 0.001) in both apo A1 and apo B100 levels of 0.06 ± 0.11 mmol/L and 0.12 ± 0.12 mmol/L, respectively. Further examination of the LDL-C:apo B100 ratio indicated a rise (p = 0.002) of 0.13 ± 0.23.


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  		Table 1. Before and after Weight and Biochemical Parameter Concentrations

 
After weight loss, glucose levels were lowered (p = 0.02) by 0.24 ± 0.59 mmol/L and insulin by 5.43 ± 5.00 mmol/L (p < 0.001). There was a reduction (p < 0.001) in leptin of 16.0 ± 7.8 ng/L and ghrelin rose (p <0.001) 204.9 ± 274.9 pg/mL. In contrast, adiponectin levels were not significantly altered by weight loss taking the group as a whole.

Ability of Weight Loss to Predict Changes in Biochemical Parameters
No significant relationship was observed (p = 0.43) between changes in weight and changes in total cholesterol (ß1 = –0.04; r2 = 0.02) nor between changes in weight and changes in LDL-C (ß1 = –0.01; r2 = 0.00, p = 0.88) and changes in weight and changes in TAG (ß1 = –0.06; r2 = 0.10, p = 0.07). Weight loss was also not predictive (p = 0.50) of changes in HDL-C (ß1 = – 0.01; r2 = 0.01).

Higher weight loss resulted in larger decreases (p < 0.001) in leptin levels (ß1 = –1.82; r2 = 0.35) and increases (p = 0.009) in adiponectin levels (ß1 = 0.62; r2 = 0.19) (Fig. 2). Changes in weight did not predict changes in glucose, insulin, or ghrelin levels.


Figure 2
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  		Fig. 2. Regression of in leptin (ng/L) (ß1 = –1.81; r2 = 0.35; p < 0.001), and adiponectin (mcg/L) (ß1 = 0.62; r2 = 0.19; p = 0.009) on weight loss (kg) after a 20 week period.

 
Ability of Initial Biochemical Parameters to Predict Weight Loss
Change in weight was best explained by initial apoB (36.2%) and LDL-C levels (13.1%) to a final r = 0.702 in forward stepwise regression. Best subset analyses indicated the same initial parameters explained 52% of the variation in weight loss (LDL-C p = 0.004 and apoB p < 0.001) and initial insulin (p = .021), TC (p < 0.001), TG (p = 0.004), HDL-C (p < 0.001) and LDL-C (p = 0.002) collectively explained 63% of the variation in weight loss. Only the initial leptin level contributed (both in forward stepwise and best subset) to final weight, where r2 = 0.208 (i.e. 20.8% variation) for p = 0.007. The analyses indicated that baseline weight and initial levels of adiponectin, leptin, and ghrelin were not as strongly associated with the extent of weight loss.

Relationship between Lipid Parameters, Glucose, Insulin, Leptin, Adiponectin, and Ghrelin
Calculation of Pearson correlations indicated some relationships between lipid parameters, glucose, insulin, leptin, adiponectin, and ghrelin. Changes in adiponectin levels were positively associated with changes in TAG levels (r = 0.41, p = 0.01) and apo A1 levels (r = 0.38, p = 0.02) (Fig. 3). Additionally, differences in leptin levels were negatively correlated with changes in TC levels (r = –0.39, p = 0.02), apo A1 levels (r = –0.41 (p = 0.01), and apo B100 levels (r = –0.34, p = 0.05) (Fig. 3). No significant relationships were found between differences in lipid parameters and changes in glucose, insulin, and ghrelin levels. There were also no significant correlations found between adiponectin, leptin, ghrelin, and insulin.


Figure 3
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  		Fig. 3. Correlations between changes in lipid parameters and changes in hormones.

 

   DISCUSSION
 
To our knowledge, our study is the only one which attempts to isolate the effect of weight loss through pre- and post-stabilization periods. A steady state was emphasized with the fact that no significant changes were observed during the stabilization periods. Additionally, the exclusion of males in this study is unique because few weight loss trials include only females. This study found that weight loss in females resulted in significant declines in glucose, insulin, leptin, increases in ghrelin, and no changes in adiponectin. The decline in glucose and insulin seen in this study are well established and consistent with findings from other weight loss studies [21–23]. However, the effect of weight loss on leptin, adiponectin, and ghrelin levels is not as clear. Only a limited number of existing studies have examined effects of weight loss on ghrelin through diet and exercise on women. The increases in ghrelin found through weight loss in the current study are similar to that found in other weight loss studies [24,25].

Although no significant differences in absolute adiponectin levels were found after weight loss in the present trial, individual increases and decreases changed such that weight loss was predictive of changes in adiponectin levels. This finding is consistent with the existing evidence which shows that adiponectin is inversely correlated with fat mass [21,26]. In addition, a trial that examined the effect of weight loss through surgical procedures found changes in BMI to be negatively associated with adiponectin (r = –0.20) [27]. The lack of studies examining the consequences of weight loss on adiponectin in women is especially noteworthy since adiponectin concentrations are gender specific; with women having higher concentrations than men [28]. An investigation of hormonal effects on adiponectin would be useful in further explaining the effect of weight loss on adiponectin levels in females.

Weight loss was also predictive of decreases in leptin in this experiment. Similar relationships were found in other studies that assessed weight loss and changes in leptin levels [24,27]. However, these prior studies were conducted in a population that had a much higher initial BMI than was used in this study, and employed surgical procedures or pharmaceutical methods to promote weight loss [24,27].

Few studies measure all of insulin, adiponectin, leptin, and ghrelin simultaneously and none examine them in the context of weight loss through diet and exercise. Though weight loss was predictive of changes in adiponectin and leptin concentrations, changes in these parameters, as well as changes in insulin and ghrelin, were not correlative. Thus, though adiponectin, leptin, insulin, and ghrelin are all involved in energy expenditure and storage, the present results show that they change independently of each other. This may indicate that each hormone contributes differently to weight loss.

Regression analyses in this study show that the amount of weight loss was not predictive of any change in lipid parameters. A meta-analysis of 70 studies by Dattilo and Kris-Etherton [4] found an association whereby TC, LDL-C, and TAG decreases and HDL-C increases for every kilogram loss. However, an earlier study by Andersen et al [29], which examined the effects of diet induced weight loss in women, found weight loss to account for no more than 6% of the variation in reductions of TC and TAG. The fact that no relationship was found between lipid parameters could have occurred because there was not enough power with the number of subjects that participated in the trial. However, the meta-analysis examined data from both men and women and the association may not be as strong in women [4]. Additionally, the associations found between percent weight change and TC, LDL-C, and HDL-C were highly insignificant; indicating an unlikely relationship between the extent of weight loss and changes in lipid parameters. We therefore suggest a threshold effect whereby, after 10% loss such as in the present study, the extent of lipid lowering produced by weight loss in itself is minimized, thus diluting any existing dose-response relationship between weight loss and lipid parameters. This is further supported by the finding by Wing and Jeffery [3] who found that decreases in weight of 10% to 15% produced cardioprotective changes in blood lipid profiles of both overweight men and women.

A notable finding of the present study was that baseline lipid and insulin levels were predictors of total weight loss, even though initial weight did not predict total weight loss. Previous research has shown a relationship between initial weight and final weight loss [13]. The lack of association between initial weight and final weight loss is unexpected since the higher energy expenditure in those with higher initial weight may result in easier weight loss through energy restriction. As well, higher initial weight may play a motivating role in weight loss. The ability of baseline insulin to predict final weight loss has been seen in other studies [14]. Trials in Pima Indians and the San Luis Valley Diabetes study have indicated that insulin resistance may limit weight gain [30,31]. Thus, the presence of initial hyperinsulinemia may be predictive of increased weight loss. No study has yet determined that baseline lipids may play a role in predicting weight loss. In this study, participants were screened to have higher baseline TC, LDL-C, and TAG concentrations and thus had knowledge of these levels. The predictive relationship found between initial lipid parameters and final weight loss may indicate the importance of patient knowledge of these risk factors as behavioural motivators for weight loss.

Such favourable changes in lipid profile may be explained by the effect of weight loss on cholesterol metabolism. Although very few studies have examined the effects of weight loss on cholesterol metabolism, those that did have indicated that weight loss may decrease cholesterol synthesis [32,33]. Endogenous production of cholesterol occurs in many cells including adipocytes and hepatocytes [34]. Cholesterol synthesis per gram of hepatic tissue has been found to be equivalent in obese and non-obese individuals [35]. However, in obesity, both adipocytes and hepatocytes increase in number, explaining the higher rates of cholesterol synthesis seen in overweight individuals [32,33]. In weight loss, the mobilization of adipose tissue stores of cholesterol during caloric restriction may result in the inhibition of hepatic cholesterol synthesis, and thus explaining a possible mechanism by which changes in blood lipid concentrations occur [4]. Further studies that examine the effect of weight loss on cholesterol metabolism are needed to strengthen this hypothesis.


   CONCLUSION
TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
ACKNOWLEDGMENTS
 REFERENCES
 
In summary, though present results show decreases in leptin and increases in ghrelin, beneficial effects of weight loss as achieve through diet and exercise were seen on blood lipid, glucose, and insulin levels of overweight and obese hyperlipidemic women. Such favourable changes in blood lipid profile likely results in decreased risk of mortality from type 2 diabetes and CVD. Additionally, knowledge of initial lipid risk factors may be behavioural motivators that predict weight loss success. Thus, moderate weight loss is a key factor in the prevention of cardiovascular disease in overweight individuals.


   ACKNOWLEDGMENTS
TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
REFERENCES
 
We would like to thank Catherine Vanstone, William Parsons, Sue Jalbert, and Robert Zakarian for their help and support. S.S. is a recipient of a Natural Science and Engineering Research Council scholarship. P.J.H.J. presently holds a Canada Research Chair in Functional Foods (University of Manitoba). K.C. presently holds a Canada Research Chair in Adipose Tissue (Laval University).


   FOOTNOTES
TOP
 FOOTNOTES
ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
This work was supported by a grant by CIHR MOP57814 to PJHJ and MOP64446 to KC.

Received July 31, 2005. Accepted May 11, 2006.


   REFERENCES
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 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 

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