Thyroid, cortisol and growth hormone levels in adult nigerians with metabolic syndrome
Ifeoma Christiana Udenze1,&, Olusola Festus Olowoselu2, Ephraim Uchenna Egbuagha1, Temitope Adewunmi Oshodi1
1Department of Clinical Pathology, College of Medicine, University
of Lagos, Nigeria, 2Department of Haematology and Blood transfusion,
of Medicine, University of Lagos, Nigeria
Ifeoma Christiana Udenze, Department of Clinical Pathology, College of Medicine,
University of Lagos, Nigeria
the similarities in presentation of cortisol excess, growth hormone deficiency,
hypothyroidism and metabolic syndrome suggest that subtle abnormalities of
these endocrine hormones may play a causal role in the development of metabolic
The aim of this study is to determine the levels of cortisol, thyroid and
growth hormones in adult Nigerians with metabolic syndrome and determine the
between levels of these hormones and components of the syndrome.
this was a case control study conducted at the Lagos University Teaching
Hospital, Lagos, Nigeria. Participants were fifty adult men and women with the
syndrome, and fifty, age and sex matched males and females without the metabolic
syndrome. Metabolic syndrome was defined based on the NCEP-ATPIII criteria.
Written Informed consent was obtained from the participants. Socio demographic
and clinical data were collected using a structured questionnaire. Venous
blood was collected after an over-night fast. The Ethics committee of the Lagos
Teaching Hospital, Lagos, Nigeria, approved the study protocol. Comparison
of continuous variables was done using the Student's t test. Correlation analysis
was employed to determine the associations between variables. Statistical
was set at P<0.05.
triiodotyronine (T3) was significantly decreased (p<0.001) and thyroxine (T4
) significantly increased ( p<0.001) in metabolic syndrome compared to healthy
controls. T3 correlated positively and significantly with waist circumference
(p=0.004), glucose (p= 0.002), total cholesterol ( p=0.001) and LDL- cholesterol
( p<0.001 ) and negatively with body mass index ( p<0.001 )and triglyceride
( p=0.026). T4 had a negative significant correlation with waist circumference
(p=0.004). Cortisol and growth hormone levels were similar in metabolic syndrome
and controls. Cortisol however had a positive significant correlation with
waist/hip ratio (p<0.001) while growth hormone correlated positively with HDL
( p=0.023)and negatively with diastolic blood pressure (p=0.049).
thyroid hormones T3 and T4 were associated with metabolic syndrome. The thyroid
hormones, cortisol and growth hormones correlated with components of the
syndrome. A therapeutic role may exit for these hormones in the management of
syndrome and related disorders.
Disorders of some endocrine hormones have features similar to the
components of the metabolic syndrome and this has led to the suggestion
that a mild degree of endocrine disorders may underlie the metabolic
syndrome phenotype [1-3]. These endocrinopathies include
disorders of cortisol, thyroid and growth hormone secretion [1-3].
Cushing's syndrome is an endocrine disorder characterised by excess cotisol levels
in blood and increased urinary cortisol excretion .
Cortisol is a glucocorticoid hormone secreted by the zona glomerulosa
cells of the adrenal cortex in response to adrenocorticotrophin
from the pituitary gland . The primary function of
cortisol is in the physiological adaptation to stress .
Through its action on glucose and lipid metabolism, cortisol ensures
adequate provision of metabolic substrates to cope with stressful
Adrenocortical hyperfunction arising from tumours of the adrenal
cortex lead to Cushing's disease and cortisol excess .
Cortisol hyperactivity mediated through an increased adipose tissue
clinical features similar to metabolic syndrome [7,8].
Cross-sectional studies have shown that individuals with raised blood pressure,
glucose intolerance or other features of the metabolic syndrome
have raised fasting plasma cortisol concentrations [9, 10].
Growth hormone promotes protein synthesis, lipid degradation and
energy metabolism, where, acting as a counter regulatory hormone,
insulin to modulate its control of carbohydrate metabolism .
A relationship between growth hormone and cortisol has been described
Growth hormone has an inhibitory effect on the 11beta-hydroxysteroid
dehydrogenase enzyme 1, responsible for activating cortisol from
inactive cortisone in
the liver and adipose tissue, hence growth hormone deficiency effectively
increases cortisol production in key target tissues of liver and
adipose tissue, promoting insulin resistance and visceral adiposity
Occult abnormalities of the thyroid gland, notably subclinical
hypothyroidism  and the sick euthyroid syndrome 
have also been linked with increased prevalence of the metabolic
syndrome and its components. The criteria defining metabolic syndrome
the National Cholesterol Education Programme-Adult Treatment Panel
III (NCEP-ATPIII)  require a combination of at
least 3 of the following 5 criteria: Abdominal circumference ≥ 102
cm in males or ≥ 88
cm in females, HDL cholesterol < 1.03 mmol/L (< 40 mg/dL) [males] or < 1.3
mmol/L (< 50 mg/dL) [females], triglycerides ≥ 1.7 mmol/L (≥150
mg/dL), blood pressure ≥ 130/85 mmHg or the patient receiving hypotensive
treatment and fasting glycaemia > 6.1 mmol/L (> 110 mg/dL). The prevalence
of metabolic syndrome has increased greatly not only in industrialized
nations but also in developing countries, reaching pandemic proportions
The treatment modality so far is the control of the individual
components of the syndrome to prevent the occurrence of cardiovascular
complications or progression to type 2 diabetes .
It is unclear whether a single endocrine abnormality triggers the cascade of
events that leads to the manifestation of the metabolic syndrome.
An understanding of related or associated mechanisms in metabolic
syndrome may change management
strategies and lead to improved outcomes. Clinical trials using
preparations of cortisol synthesis inhibitor such as ketoconazole
and recombinant growth
hormone are still on going in white populations [19,20].
There are few studies investigating the role of cortisol, thyroid
and growth hormones in adult Nigerians with metabolic syndrome.
This study aims to
determine the levels of cortisol, thyroid and growth hormones in
adult Nigerians with metabolic syndrome and determine the relationship
between levels of
these hormones and components of the syndrome.
This is a cross sectional study of fifty adult men and women with
metabolic syndrome and fifty, age and sex matched males and females without
metabolic syndrome. The Ethical Research and Review Committee of the hospital
approved the study protocol and informed consent was obtained from the participants.
The study participants were patients attending The Obesity and Metabolic Clinic
of the Lagos University Teaching Hospital. Adult men and women between the
age of 30 and 70 years who agreed to participate in the study were consecutively
recruited. Socio demographic and clinical data were obtained from the participants
using a structured questionnaire. Anthropometric measurements such as weight,
height, waist and hip circumference and blood pressure readings were taken.
Lipid profile results were also determined. The diagnosis of the metabolic
syndrome was based on the NCEP-ATPIII criteria .
Subjects who didn't meet the criteria for metabolic syndrome were matched for
age and sex with the cases and recruited as controls. The inclusion criteria
included adult males and females between 30 and 70 years of age who had
any three of the following: Abdominal circumference ≥ 102 cm in males
or ≥ 88 cm in females, HDL cholesterol < 1.03 mmol/L (< 40 mg/dL)
(females) or < 1.3 mmol/L (< 50 mg/dL) [females], triglycerides ≥ 1.7
mmol/L (≥ 150 mg/dL), blood pressure ≥ 130/85 mmHg or the patient
receiving hypotensive treatment and fasting glycaemia > 6.1 mmol/L (> 110
Persons with diabetes and pregnant women were excluded from the study.
The study participants reported on the morning of the study after an overnight
(10-12 hours) fast. 5 millilitres of venous blood was collected from the
ante cubital vein and transferred into plain tubes for lipid profile, growth
hormone, cortisol and free T4, free T3 and TSH assays and into fluoride
oxalate tubes for glucose analysis. Abdominal obesity was determined by
measurement of the waist circumference. The measurement was taken at the
end of several consecutive natural breaths, at a level parallel to the floor,
midpoint between the top of the iliac crest and the lower margin of the
last palpable rib in the mid axillary line . The
hip circumference was measured at a level parallel to the floor, at the
largest circumference of the buttocks .
The blood pressure was determined using the Accoson's Mercury Sphygmomanometer
(cuff size 15×43cm). The subjects were seated and rested for 5 minutes before
measurement. The systolic blood pressure was taken at the first Korotkoff
sound and diastolic at the fifth Korotkoff sound .
The total, LDL, HDL cholesterol and triglyceride were determined on fasting
serum samples and glucose concentrations were determined from fasting fluoride
oxalate plasma using reagents from Randox Laboratories Limited, Antrim,
UK, BT 29 4QY, on semiautomatic biochemistry analyser BS3000P-Sinnowa Medical
Science and Technology Company limited, Nanjing, China (211135). Serum levels
of growth hormone, cortisol, free T4, free T3, and TSH were determined using
reagents from Biovendor Laboratories, 62100 Brno, Czech Republic by an enzyme
linked immunoassay technique  on Acurex Plate Read
- Acurex Diagnostics, Ohio, USA (419-872-4775). The data were analysed
using the IBM SPSS version 20.0 package. Independent student's t test was
employed to test the differences in the mean values for the continuous variables.
Spearman's correlation analysis was employed to determine the association
between variables. Statistical significance was set at p < 0.05.
Fifty subjects met the criteria for metabolic syndrome and were recruited
as cases. Another fifty subjects without metabolic syndrome were
matched for age and sex with the cases and recruited as controls. The study
included twenty men and thirty women with metabolic syndrome and
age and sex matched controls.
Table 1 shows
the age, sex and ethnic distribution of the study participants. The mean age
of the cases with metabolic syndrome was 47.16±13.4 years and 46.79±12.7 years
for the controls. Two-thirds of the study participants were between 30-50 years
of age, two-thirds were females and majority belonged to the Yoruba tribe. The
age and sex matched cases and controls however did not differ in their age, sex
and ethnic characteristics.
Table 2 shows
the demographic characteristics of the study participants. Over sixty percent
of the study participants had tertiary education, over seventy percent were Christians
and most were married. The study participants did not differ in their demographic
Table 3 shows
the nature of work and lifestyle habits of the study participants Almost eighty
percent of the study participants had sedentary lifestyles though majority neither
smoked nor took alcohol. The study participants did not differ in their lifestyle
Table 4 shows
the clinical and laboratory characteristics of the study participants. There
was a statistically significant difference in the diastolic blood pressure values
between the groups with and without metabolic syndrome. The various measures
of obesity also differed significantly between the two groups. Of the lipid profile
parameters, only HDL cholesterol differed significantly between the groups.
Table 5 shows
the levels of the endocrine hormones in subjects with and without metabolic syndrome.
Free T3 was significantly lower and free T4 significantly higher in the metabolic
syndrome group compared to controls. The group with metabolic syndrome had higher
cortisol and lower growth hormone values than the control subjects though the
differences were not statistically significant.
Table 6 shows
the correlation of the endocrine hormones with components of the metabolic syndrome
Free T3 had a direct relationship with waist circumference, glucose, total cholesterol
and LDL cholesterol and an inverse relationship with BMI and triglyceride. T3
had an inverse relationship with waist circumference. Growth hormone correlated
positively with HDL and negatively with diastolic blood pressure while cortisol
has a strong direct correlation with waist/hip ratio
This study reports a statistically significant decrease in serum free
triiodotyronine (T3) and a statistically significant increase in serum
free thyroxine (T4 ) in people with metabolic syndrome compared to
suggesting that some degree of thyroid hypofunction is associated with
metabolic syndrome [2, 13]. A study
from Nigeria by Ogbera et al;  reported a prevalence
of 40% for metabolic syndrome in patients with hypothyroidism. In our
study, T3 also correlated with most of the features of metabolic syndrome,
positively with waist circumference, glucose, total cholesterol and
LDL- cholesterol and negatively with body mass index and triglyceride.
review by Iwen et al;  showed convincing evidence
for a major impact of thyroid function on all components of the metabolic
syndrome. Thyroid dysfunction is associated with changes in body weight
and composition, body temperature, and basal metabolic rate .
Both subclinical and overt hypothyroidism are frequently associated
with weight gain while hyperthyroidism has been associated with weight
to catabolic effects on muscle and adipose tissue 
explaining the inverse relationship between T3 and BMI reported in
this study. In this study, waist circumference, a surrogate marker
of abdominal obesity,
correlated positively with T3 and negatively with T4. This may be because
leptin, an adipokine which functions through the hypothalamus to decrease
adipose tissue mass, activates thyroidal 5'deiodinase enzyme, increasing
the conversion of T3 from T4 [27, 28].
Thyroid hormones play important roles in the regulation of glucose and lipid
metabolism . In the fasting state, thyroid hormones,
together with other counter insulin hormones stimulate hepatic gluconeogenesis
resulting in increased blood glucose .
Thyroid hormones affect many of the enzymes involved in cholesterol synthesis
and lipid metabolism which explains findings from this study. Thyroid hormones
induce the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which is
the first step in cholesterol biosynthesis. T3 upregulates LDL receptors by controlling
the LDL receptor gene activation, this it does by the direct binding of T3 to
specific thyroid hormone responsive elements [30
]. T3 also
controls the sterol regulatory element-binding protein-2, which in turn regulates
LDL receptor's gene expression [31
]. Furthermore, T3 up-regulates
apolipoprotein AV, which plays a major role in TG regulation with the effect
of decreasing TG levels by decreasing hepatic production of triglyceride from
]. Thyroid hormones can
also influence HDL metabolism by increasing cholesteryl ester transfer protein
In this study, cortisol and growth hormone levels were not significantly different
in the groups with and without metabolic syndrome, although they correlated with
some features of metabolic syndrome. A similar study in obese children and adolescents
] reported a weak association between cortisol and metabolic
syndrome components. A study in South Asians [36
comparable cortisol results between metabolic syndrome and healthy controls but
reported strong associations between cortisol and most of the components of metabolic
syndrome. This study reports a positive and significant correlation between cortisol
and waist/hip ratio (WHR) alone, WHR being a surrogate marker for abdominal obesity.
Albeit, it has been suggested that a critical factor in the association between
obesity, dyslipidaemia, hypertension, type 2 diabetes and cardiovascular morbidity,
features of metabolic syndrome, is the intraabdominal fat mass [3
Cortisol hyperactivity produces features of metabolic syndrome mediated through
an enlarged visceral fat mass, cortisol being a powerful stimulator of visceral
fat accumulation by its effect on lipoprotein lipase receptors which are highly
concentrated in visceral adipose tissue [8
The expanded abdominal fat mass will result in insulin resistance through increased
production of the adipokine, resistin [38
]. Resistance to
the actions of insulin on glucose and carbohydrate metabolism will give rise
to the classical features of metabolic syndrome [39
also potentiates the lipolytic action of the β adrenergic receptors which
also are concentrated in visceral adipose tissue, increasing free fatty acid
flux and promoting insulin resistance [40
Individuals with growth hormone deficiency have central obesity, insulin resistance
atherosclerosis and increased mortality from cardiovascular diseases resulting
both from growth hormone's pivotal role in lipid degradation and energy metabolism
and from its effect on cortisol metabolism [12
In this study, growth hormone correlated positively with HDL cholesterol and
negatively with diastolic blood pressure. Some studies have reported dyslipidaemias
in individuals with growth hormone deficiency with increased total cholesterol,
LDL- cholesterol, triglyceride and decreased HDL- cholesterol [41
Improvement in lipid parameters and diastolic blood pressure have also been recorded
after growth hormone therapy in patients with growth hormone deficiency [3
Lower levels of T3 were associated with metabolic syndrome and its components in Nigerians. The finding of similar cortisol and growth hormone levels in metabolic syndrome and in healthy controls does not support a major role for cortisol and growth hormone in the pathogenesis of metabolic syndrome in Nigerians. The relationship of these hormones with components of the syndrome however suggests the possibility of a therapeutic role for these hormones in the management of metabolic syndrome. Interventional studies are therefore needed to further evaluate these relationships.
What is known about this topic
- Endocrinopathies involving cortisol, growth hormone and the thyroid gland produce features of metabolic syndrome.
What this study adds
- In adult Nigerians, individuals with metabolic syndrome have abnormalities of thyroid hormone secretion consistent with lower free T3 and higher free T4 concentrations than individuals without metabolic syndrome;
- In adult Nigerians with metabolic syndrome, serum levels of cortisol, thyroid and growth hormone correlate with components of metabolic syndrome and may suggest a therapeutic role for these hormones in the management of the syndrome.
The authors declare no competing interest
All the authors contributed substantially to the conception and design of the study, acquisition of data, and its analysis and interpretation, drafting the article and revising it for important intellectual content; and final approval of the version to be published.
Table 1: age, sex and ethnic distributions of the Study participants
Table 2: demographic characteristics of the Study participants
Table 3: lifestyle habits and nature of work of the study participants
Table 4: clinical and laboratory parameters of the study participants
Table 5: the levels of the endocrine hormones in subjects with and without metabolic syndrome
Table 6: correlation of the endocrine hormones with components of the metabolic syndrome
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