|Year : 2014 | Volume
| Issue : 1 | Page : 58-64
Assessment of serum leptin, atherogenic lipids, glucose level, insulin resistance and metabolic syndrome in patients with skin tags
Naglaa F Agamia1, Salwa H Gomaa2
1 Department of Dermatology, Venereology & Andrology, Main University Hospital, Faculty of Medicine, Alexandria, Egypt
2 Department of Chemical Pathology, Medical Research Institute, Alexandria University, Alexandria, Egypt
|Date of Submission||24-Mar-2014|
|Date of Acceptance||21-May-2014|
|Date of Web Publication||24-Jul-2014|
Naglaa F Agamia
MD, PhD, Department of Dermatology, Venereology & Andrology, Faculty of Medicine, Alexandria University, Alexandria-21131
Source of Support: None, Conflict of Interest: None
Skin tags (STs) are papillomas commonly found on the neck and on the axillae of middle-aged and elderly people. Metabolic syndrome is a complex of interrelated risk factors for cardiovascular disease and diabetes. Epidemiologic studies on different ethnic populations have indicated that hyperleptinaemia and leptin resistance are strongly associated with metabolic syndrome.
The aim of the study was to investigate the relationship between serum leptin, homoeostasis model assessment of insulin resistance (HOMA-IR) and atherogenic lipid in patients with STs and to compare them with the levels in healthy controls.
This study included 90 participants, 60 ST patients and 30 apparently healthy age-matched and sex-matched controls. Fasting glucose level, insulin level and insulin resistance were estimated in addition to cholesterol, triglycerides, high-density lipoprotein, leptin and HOMA-IR levels.
The univariate analysis showed that waist circumference, BMI, fasting glucose, insulin levels, insulin resistance, cholesterol, triglycerides, HDL, leptin and HOMA-IR levels were significantly higher in ST patients compared with controls (P < 0.001). The multivariate analysis between metabolic syndrome components and ST showed that only high triglyceride levels and low HDL levels were significantly associated with ST. Multivariate linear regression analysis of the predictors of high plasma leptin levels showed that high triglyceride levels and low HDL levels were significant predictors.
The results of this study suggested that the presence of both ST and hyperleptinaemia in patients with STs may be associated with high levels of triglycerides and low levels of HDL, and this could suggest that changing the life style of patients with ST may have a beneficial role.
Keywords: Atherogenic lipids, leptin, metabolic syndrome, skintags
|How to cite this article:|
Agamia NF, Gomaa SH. Assessment of serum leptin, atherogenic lipids, glucose level, insulin resistance and metabolic syndrome in patients with skin tags. Egypt J Dermatol Venerol 2014;34:58-64
|How to cite this URL:|
Agamia NF, Gomaa SH. Assessment of serum leptin, atherogenic lipids, glucose level, insulin resistance and metabolic syndrome in patients with skin tags. Egypt J Dermatol Venerol [serial online] 2014 [cited 2017 Aug 20];34:58-64. Available from: http://www.ejdv.eg.net/text.asp?2014/34/1/58/137314
| Introduction|| |
Skin tags (STs) are soft, small, skin-coloured to dark brown sessile or pedunculated papillomas commonly occurring on the neck, frequently seen on the axilla and eyelids and less often on the trunk and groin. They are also named soft fibromas, achrocordons or fibroepithelial polyps . The definite aetiology of STs is still unknown. Skin rubbing , hormonal imbalance , obesity , metabolic syndrome  and other conditions have been reported as contributing factors.
Leptin, a 16-kDa protein, which is a product of the obese gene, is involved in the regulation of appetite and energy expenditure. Leptin is produced mainly by the adipocytes, and low levels have been detected in gastric fundic epithelium, intestine and skeletal muscle. The protein circulates at concentrations proportional to body fat and decreases body weight by inhibiting food intake and inducing thermogenesis . Recently, leptin has been reported to stimulate the proliferation of various cell types and is considered to be a new growth factor . Plasma leptin displays a strong association with cardiovascular risk factors, including obesity, insulin resistance, hypertension, dyslipidaemia, hyperuricaemia and inflammatory markers .
Insulin resistance is a state in which a given concentration of insulin produces a less-than-expected biological effect. Obesity is the most common cause. This is followed by compensatory hyperinsulinaemia to maintain normal glucose and lipid homoeostasis . Different methods are available for assessment of insulin resistance, of which calculation of the homoeostasis model assessment of insulin resistance (HOMA-IR) provides a useful approach . Insulin resistance syndrome or metabolic syndrome is a collection of health risks that increase the chance of developing heart disease, stroke and diabetes. Various risk factors have been included and the factors generally accepted as being characteristic of this syndrome include abdominal obesity, raised blood pressure, atherogenic dyslipidaemia and insulin resistance with or without glucose intolerance .
The present study was designed to investigate serum leptin, HOMA-IR, atherogenic lipids, glucose levels and metabolic syndrome in patients with STs and to compare them with these markers levels in healthy controls.
| Patients|| |
This study was conducted on 90 candidates who were divided into two groups. Group 1 included 60 patients suffering from STs on different sites such as neck, axilla and eyelids. Group 2 enrolled 30 age-matched and sex-matched individuals with apparent normal skin. All participants were selected from the outpatient clinic of the Department of Dermatology, Venereology & Andrology, Main University Hospital, Faculty of Medicine, Alexandria University.
Exclusion criteria were pregnant or lactating women who could affect the outcome of the study. Patients taking any drug (such as antidiabetic, antihypertensive and antiuricaemic drugs) that could alter leptin or glucose metabolism were also excluded. The study protocol conformed to the ethical guidelines of Alexandria University and was approved by the Local Ethical Committee of Scientific Research. Before initiation, every patient was informed about the aim of the study.
| Materials and Methods|| |
All patients and controls were subjected to full history taking, family history and general examination. Waist circumference was noted and BMI was determined using the following equation: weight (kg)/height (m 2 ). Participants with BMI 19-25 kg/m 2 were considered normal, 26-29 kg/m 2 as overweight and equal or greater than 30 kg/m 2 as obese . For laboratory studies, venous blood samples were taken from all studied groups after 12 h fasting at 8:00-9:00 am. They were drawn in vacutainer plain tubes and centrifuged at 4000 rpm for 10 min, stored at -70°C and thawed just before analysis.
- Routine laboratory investigations in patients and controls included: Fasting blood glucose, serum uric acid level and total lipid profile including total triglyceride, total cholesterol, high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol.
- Assessment of fasting insulin for estimation of HOMA-IR: Fasting insulin was measured in all samples by chemiluminescence on immunolit 1000 after 8 h fasting for estimation of HOMA-IR. Estimation of insulin resistance by estimation of HOMA-IR was calculated as follows: Serum insulin (μIU/ml) Χ fasting blood glucose (mg/dl)/405 .
- EDTA plasma for estimation of glycated haemoglobin (HBA1C) was measured during column chromatography with cation-exchange resin tubes.
- Leptin serum level was determined by enzyme-linked immunosorbent assay (ELISA) (R&D Systems, Oxford, U.K.).
Metabolic syndrome was determined using the International Diabetes Federation (IDF) including five constituents or markers of the metabolic syndrome. These are central obesity [elevated waist circumference (men ≥94 cm and women ≥80 cm)], elevated triglycerides (≥150 mg/dl), reduced HDL (men <40 mg/dl, women <50 mg/dl), elevated blood pressure (≥130/85 mmHg) and elevated fasting glucose (≥100 mg/dl). IDF suggested that the diagnosis of the metabolic syndrome is made in the presence of more than three of these risk markers .
| Results|| |
This study enrolled 90 candidates, who were divided into two groups: group I included 60 patients (34 men and 26 women) suffering from variable numbers of STs, with a mean of 45.56 ± 15.26 years of age, who were compared with group II including 30 control individuals (12 men and 18 women) not suffering from STs, with a mean of 35.10 ± 12.90 years of age. Twenty-seven patients were obese, 25 were overweight and eight patients had normal BMI. Waist circumference was significantly high in the patient group (111.88 ± 25.58) than in the control group (99.90 ± 13.99). The number of patients with noninsulin-dependent diabetes mellitus was 45 (75%), whereas none of the control individuals were diabetic.
Comparison between the two studied groups according to the criteria of metabolic syndrome
It was found that fasting blood sugar was significantly higher in the patients group (mean was 112.80 ± 40.06 mg/dl) than in the control group (the mean was 89.80 ± 13.37 mg/dl). Diastolic and systolic blood pressures and serum triglyceride, total cholesterol and LDL levels were higher in the patients group. Insulin serum level in the patients group was significantly higher (the mean was 10.72 ± 11.80 μIU/ml) than their serum levels in the control group (mean was 4.51 ± 4.64 μIU/ml).
The mean serum leptin level in male patients was 191.94 ± 96.47 ng/ml and in female patients was 91.68 ± 58.0 ng/ml, and the difference was statistically significant (P < 0.001). Serum leptin level in patients was significantly higher than in the control group (P < 0.05, P = 0.001), whereas the difference between plasma glycated haemoglobin level in the patients and its plasma levels in the control group was statistically nonsignificant (P > 0.05, P = 0.072) [Table 1].
|Table 1: Comparison between the two studied groups (patients with skin tags and controls) according to serum leptin level and glycated haemoglobin in plasma|
Click here to view
Both the patients group and the control group were divided into three subgroups regarding BMI and were compared according to serum leptin level
The comparison of serum leptin levels between the patients group and BMI-matched controls revealed significant differences between normal BMI patients and normal BMI controls, obese patients and obese controls and between overweight patients and overweight controls. Using the post-hoc test, the highest serum leptin levels were found in obese patients with significant difference when compared with normal BMI patients but with insignificant difference when compared with overweight patients. The same was true for the control group, where the highest serum leptin levels were found in the obese control group with significant difference when compared with normal controls but with insignificant difference when compared with overweight controls [Table 2].
|Table 2: Comparison between the patients and control groups according to serum leptin level|
Click here to view
With respect to HOMA-IR, it was significantly higher in all three groups of patients compared with their BMI-counterpart controls [Table 3]. Post-hoc test revealed insignificant differences between normal BMI patients and overweight patients, with a P value of 0.644, and between overweight patients and obese patients, with a P value of 0.609, and it revealed significant difference between normal BMI patients and obese patients, with a P value of 0.006. Post-hoc test revealed insignificant differences between normal BMI controls and overweight controls, with a P value of 0.177, between overweight controls and obese controls, with a P value of 0.096 and between normal BMI controls and obese controls, with a P value of 1.000.
In all, 37 (61.5%) patients fulfilled the criteria of metabolic syndrome and 23 patients did not. The mean serum leptin level in patients without metabolic syndrome was 132.30 ± 81.71 ng/ml, whereas in patients with metabolic syndrome the mean serum leptin level was 213.79 ± 97.34 ng/ml, and this difference was statistically significant (P = 0.001) [Figure 1]. The mean HOMA-IR level in patients without metabolic syndrome was 2.56 ± 3.46 ng/ml, but this level was 3.49 ± 2.47 ng/ml in patients with metabolic syndrome, and this difference was statistically significant (P = 0.001) [Figure 2]. The mean serum level of HBA1C was 6.96 ± 2.22 mmol/l in patients with metabolic syndrome and its level in patients without metabolic syndrome was 5.65 ± 0.81 mmol/l (P = 0.006), and this difference was statistically significant.
|Table 3: Comparison between the different studied groups according to HOMA-IR|
Click here to view
In the present study, there was a statistically significant positive correlation between serum leptin level and HOMA-IR in obese patients [Figure 3]. In contrast, there was no statistically significant correlation between serum leptin level and glycated haemoglobin (HBA1C) in the obese patients.
Regarding the relationship of serum leptin with other investigatory criteria, there was statistically significant correlation between serum leptin level and fasting glucose level and serum uric acid, but there was no significant correlation between serum leptin level and total cholesterol, total triglycerides, HDL, LDL and waist circumference. In contrast, there was statistically significant correlation between HOMA-IR and fasting blood sugar, total cholesterol, serum uric acid, total triglycerides, LDL and waist circumference, but there was no significant correlation between HOMA-IR and HDL.
| Discussion|| |
STs are common benign lesions that are composed of loose fibrous tissue and occur mainly on the neck and major flexures as small soft, pedunculated protrusions. These lesions are very common, particularly in women at menopause or later . Obesity is a factor that has been associated with the development of ST .
In the present study, STs were mostly found on the neck, axillae, back and less often on the eyes, face, thighs and under the breast. The colour was skin coloured or brownish, the size ranged between 5 and 10 mm and the number was either one, two, three or multiple. This is in agreement with the studies by Chiritescu et al.  and El Safoury et al.  who observed STs commonly occurring on the neck, frequently seen on the axilla and eyelids and less often on the trunk and groin. Our study proved that there was no relationship of STs with both age and sex. This is in agreement with the studies by Gorpelioglu et al.  and Chiritescu et al. who found an equal prevalence of STs in male and female population. Hidalgo  reported that the frequency and number increase with advancing age and obesity.
El Safoury et al.  suggested the possible role of androgen and oestrogen receptors in aetiogenesis of STs and proposed that the neck is an androgen-dependent area just similar to the axillae and the groins.
Leptin displays a strong association with obesity and insulin resistance . There are some studies that explain the role of leptin in development of STs. Direct proliferative effects of leptin on mouse and human keratinocytes have been reported . The impact of leptin as a keratinocyte mitogen in skin repair has been also studied . Moreover, leptin has been found to stimulate the proliferation of various cell types, and is therefore considered a new growth factor . In this study, serum leptin was significantly higher in female patients; this was in agreement with the study by Gorpelioglu et al.  and other studies , which found that female patients had significantly higher fasting serum leptin levels than male patients because of the increase in total fat mass.
In the present study, serum leptin levels were found to be significantly higher in each group of patients in comparison with their counterpart BMI-matched controls with no STs. This supports the role of leptin in STs; this is in agreement with the study by El Safoury et al.  who previously reported increased tissue leptin levels in ST lesions compared with normal skin, and they reasoned that to leptin induction of cellular proliferation.
We also proved in this study using the post-hoc test that serum leptin levels were significantly higher in obese patients compared with normal BMI and overweight individuals in both ST patients and controls. This is in agreement with the study by Shaheen et al.  who supported the role of obesity in induction of serum leptin irrespective of the presence of STs. Obese individuals are largely leptin tolerant or leptin resistant, and the use of leptin sensitizers for the treatment of obesity and weight loss maintenance is being greatly anticipated .
Gorpelioglu et al.  , in contrast, found no significant difference in serum leptin levels between overweight patients and their BMI-matched controls, but a significant positive correlation was found between serum leptin level in obese ST patients and their BMI-matched controls, supporting the association of leptin with obesity .
It was proved that insulin resistance is an important risk factor in the development of metabolic syndrome, which is a cluster of disorders comprising glucose intolerance, dyslipidaemia, hypertension and dysfibrinolysis, and is associated with type 2 diabetes and cardiovascular disease; the presence of multiple STs was strongly associated with insulin resistance .
In this study, HOMA-IR, which is considered an accurate method for assessing hyperinsulinaemia and insulin resistance, was significantly higher in all three groups of STs patients compared with their BMI-counterpart controls. This is in contrast with the study by Marthur et al.  who estimated insulin resistance in 10 patients with multiple ST and 10 control individuals matched for age, sex and body weight. They concluded that ST are not markers of insulin resistance and it is possible that epidermal growth factor or other growth factors may play a role in the pathogenesis of ST. on the other handThis is in agreement with the study by Tamega et al.  who proved in their study that the presence of multiple STs was strongly associated with insulin resistance. Hence, it is recommended to assess HOMA-IR in patients with STs for early detection of insulin resistance.
HOMA-IR serum level was found to be significantly higher in obese patients with respect to normal BMI, and this might support the relationship of insulin resistance with obesity. Cnop et al.  reported that insulin resistance is an important risk factor in the development of metabolic syndrome, and hence insulin resistance could be assessed using HOMA-IR. Therefore, they suggested that the assessment of HOMA-IR in patients with STs provides higher value than serum leptin in proving the relationship between metabolic syndrome and STs.
In this study, it was found that fasting blood sugar and Insulin serum levels were significantly higher in the patients group compared with the control group; the number of patients with noninsulin-dependent diabetes mellitus was 45 (75%), but none of the control individuals were diabetic.
There are few reports in the literature about the association of STs with diabetes mellitus and insulin levels. Allegue et al.  reported that multiple STs have been associated with abnormalities in the glucose, specifically type 2 diabetes, hyperinsulinaemia and insulin metabolism resistance.
Sudy et al.  suggested that the relationship of the circulating insulin levels with formation of STs is perhaps because of an insulin-mediated effect on epidermal proliferation by activation of insulin-like growth factor 1 receptors, which act in certain areas of skin folds (neck, axillae, groins, lids). Moreover, it was believed that, when hyperinsulinaemia interacts with epidermal keratinocytes, the result is acanthosis nigricans, which is a known cutaneous marker of tissue resistance to insulin.
Norris et al.  suggested that raised circulating insulin levels are associated with formation of STs and that STs are more closely related to fasting insulin than to fasting glucose levels.
There are only a few number of studies about the relationship between ST and atherogenic lipid profile. Crook  investigated serum lipid profile in four patients with ST and found increased serum triglyceride and decreased HDL cholesterol. In yet another study, Erdogan et al. found increased total cholesterol in 36 patients with ST when compared with 22 healthy controls. In our study, total cholesterol levels and LDL serum levels were higher in patients with ST when compared with the healthy control group, suggesting the screening of STs patients for triglycerides and HDL and that changing the life style of these patients may have a beneficial role.
We found serum leptin levels to positively correlate with HOMA-IR in obese STs patients and obese controls; this finding suggests the relationship between leptin levels and insulin resistance in obesity. This is in agreement with the study by Muller et al.  who linked leptin to the pathophysiology of insulin resistance in obesity and attributed this to the inhibition of insulin receptor kinase activity and phosphorylation of insulin receptor substrate-1, resulting in impairment of metabolic action of insulin in the adipocytes. The amount of body fat was suggested to have an effect on insulin sensitivity mostly because of reduction in insulin receptor substrate-1 expression in the adipocytes.
In the present study, most STs patients (61.5%) fulfilled the criteria of metabolic syndrome. Leptin and HOMA-IR revealed higher values in patients with metabolic syndrome. Searching for the presence of metabolic syndrome in patients with STs seems therefore to be of great benefit. Esteghamati et al.  in their study demonstrated the contribution of serum leptin to metabolic syndrome.
On the basis of the results obtained in this study, we can conclude that serum leptin displays some association with obesity and insulin resistance and that the number and extent of STs increase with the increase in BMI and multiple STs may therefore be considered as a diagnostic clue towards the possible presence of metabolic syndrome. Their presence may help early detection of at-risk patients with the possibility of diagnosis, treatment or even prevention of the syndrome with its sequel. Assessment of HOMA-IR in patients with STs is also recommended for early detection of insulin resistance.
| Acknowledgements|| |
Conflicts of interest
There are no conflicts of interest.
| References|| |
|1.||Chiritescu E, Maloney E. Achrochndrons as a presenting sign of nevoid basal cell carcinoma syndrome. J Am Acad Dermatol 2001; 44 :789-794. |
|2.|| Allegue F, Fachal C, Pérez- Pérez P. Friction induced skin tags. Dermatol Online J 2008; 14 :18. |
|3.|| Ginarte M, Garcia-Caballero T, Fernandez-Redondo V, Beiras A, Toribio J. Expression of growth hormone receptor in benign and malignant cutaneous proliferative entities. J CutanPathol.2000; 27 :276-282 |
|4.|| Hidalgo G. Dermatological complications of obesity. Am J Clin Dermatol 2002; 3 :497-506. |
|5.|| Sari R, Akman A, Alpsoy E, Balci MK. The metabolic profile in patients with skin tags. Clin Exp Med 2010; 10 :193-197. |
|6.|| Erdogan BS, Aktan S, Rota S, Ergin S, Evliyaoglu D. Skin tags and atherosclerotic risk factors. J Dermatol 2005; 32 :371-375. |
|7.|| Ahima RS, Osei SY. Leptin signaling. Physiol Behav 2004; 81 :223-241. |
|8.|| Zhao SP, Wu ZH. Atorvastatin reduces serum leptin concentration in hypercholesterolemic rabbits. Clin Chim Acta 2005; 360 :133-140. |
|9.|| Haas J, Biddinge S. Dissecting the role of insulin resistance in the metabolic syndrome. Curr Opin Lipidol 2009; 20 :206-210. |
|10.||1Matthews D, Hosker J, Rudenski A. Homeostasis model assessment: insulin resistance and cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28 :412-419. |
|11.||1Eckel R, Grundy S, Zimmet P. The metabolic syndrome. Lancet 2005; 365 :1415-1428. |
|12.||1Daviglus M, Liu K, Yan L. Body mass index in middle age and health related quality of life in older age. Arch Intern Med 2003; 163 :2448-2455. |
|13.||1Katsuki A, Sumida Y, Gabazza E. Homeostasis model assessment is a reliable indicator of insulin resistance during follow-up of patients with type 2 diabetes. Diabetes Care 2001; 24 :362-365. |
|14.||1Alberti KGMM, Zimmet P, Shaw J. Metabolic syndrome - a new world-wide definition. A Consensus Statement from the new International Diabetes Federation. Diabet Med 2006; 23 :469-480. |
|15.||1Marcie R. Skin tags. In: Rook A, Wilkinson DS, Ebling FJ, editors. Texbook of dermatology. 6th ed. Oxford: Blackwell Scientific Publications; 1998. 1661. |
|16.||1Wu DM, Shen MH, Chu NF. Relationship between plasma leptin levels and lipid profiles among school children in Taiwan - the Taipei Children Heart Study. Eur J Epidemiol 2001; 17 :911-916. |
|17.||1El Safoury O, Fawzi M, Abdel Hay R. Increased tissue leptin hormone level and mast cell count in skin tags: a possible role of adipoimmune in the growth of benign skin growths. Indian J DermatolVenereol Leprol 2010b; 76 :538-542. |
|18.||1Gorpelioglu C, Erdal E, Ardicoglu Y, Adam B, and Sarifakiogl E. Serum leptin, atherogenic lipids and glucose levels in patients with skin tags. Indian J Dermatol 2009; 54 :20-22. |
|19.||1Seufert J. Leptin effects on pancreatic beta cell gene expression and function. Diabetes 2004; 53 :8152-8158. |
|20.||2Goren I, Pfeilschifter J, Frank D. Determination of leptin signaling pathways in human and murine keratinocytes. Biochem Biophys Res Commun 2003; 303 :1080-1085. |
|21.||2Stallmeyer B, Kämpfer H, Podda M, Kaufmann R, Pfeilschifter J, Frank S.A novel keratinocyte mitogen: regulation of leptin and its functional receptor in skin repair. J Invest Dermatol 2001; 117 :98-105. |
|22.||2Aurwex J, Steals B. Leptin. Lancet 1998; 353 :737-742. |
|23.||2Saad MF, Damani S., Gingerich RL, Riad-Gabriel MG, Khan A, Boyadjian R, et al, Kamdar V.Sexual dimorphism in plasma leptin concentration.J ClinEndocrinolMetab 1997; 82 :579-584. |
|24.||2Shaheen MA, NS, Abdel Fattah, Sayed YA, Saad AA. Assessment of serum leptin, insulin resistance and metabolic syndrome in patients with skin tags. J Eur Acad Dermatol Venereol 2012; 26 :1552-1557. |
|25.||2Esteghamati A, Noshad S, Khalilzadeh O, Morteza A, Nazeri A, Meysamie A, et al.Contribution of serum leptin to metabolic syndrome in obese and nonobese subjects. Arch Med Res 2011; 42 :244-251. |
|26.||2Mathur SK, Bhargava P. Insulin resistance and skin tags. Dermatology 1997; 195 :184. |
|27.||2Tamega A, Aranha A, Guiotoku M, et al. Association between skin tags and insulin resistance. An Bras Dermatol 2010; 85 :25-31. |
|28.||2Cnop M, Landchild M, Vidal J, et al. The concurrent accumulation of intra-abdominal and subcutaneous fat explains the association between insulin resistance and plasma leptin concentrations. Diabetes 2002; 51 :1005-1015. |
|29.||2Sudy E, Urbina F, Maliqueo M, Sir T. Screening of glucose/insulin metabolic alterations in men with multiple skin tags on the neck. J Dtsch Dermatol Ges 2008; 6 :852-855. |
|30.||3Norris PG, McFadden J, Gale E, Griffiths WA. Skin tags are more closely related to fasting insulin than fasting glucose levels.Acta dermato-venereologica. "Acta Derm Venereol. 1988; 68(4) :367-8. |
|31.||3Crook MA. Skin tags and atherogenic lipid profile. J Clin Pathol 2000; 53 :873-874. |
|32.||3Muller G, Fort J, Gerl M, et al. Leptin impairs metabolic actions of insulin in isolated rat adipocytes. J Biol Chem 1997; 272 :10585-10593. |
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3]