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Sanjer S, Bhagyamma S N, Abdul Majeed M. Thyroid hormonal variations: An overlooked factor in type 2 diabetes mellitus. jcbr 2025; 9 (3) :27-31
URL: http://jcbr.goums.ac.ir/article-1-517-en.html
URL: http://jcbr.goums.ac.ir/article-1-517-en.html
1- Department of Biochemistry, All India Institute of Medical Sciences (AIIMS), Mangalgiri, Andhra Pradesh, India
2- Department of Biochemistry, Government Medical College, Anantapuramu, Andhra Pradesh, India
3- Department of Pharmacology, Government Medical College Paderu, Andhra Pradesh, India ,drmamajeed@yahoo.com
2- Department of Biochemistry, Government Medical College, Anantapuramu, Andhra Pradesh, India
3- Department of Pharmacology, Government Medical College Paderu, Andhra Pradesh, India ,
Keywords: Type 2 Diabetes Mellitus, Hypothyroidism, Glycosylated Hemoglobin A1c, Thyroid Stimulating Hormone, Endocrine system, Thyroid dysfunction
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Data analysis was conducted using SPSS software version 25.0. Continuous variables were reported as the mean ± standard deviation, while categorical variables were presented as percentages. Statistical relationships were assessed using Pearson's correlation for continuous data and the chi-square (χ²) test for categorical data.
Results
The study cohort comprised 58% female and 42% male participants (Mean age = 52.4 ± 10.2 years), with a mean duration of T2DM exceeding 7 years (7.1 ± 3.5 years). T2DM patients demonstrated an elevated mean HbA1c value of 8.2 ± 1.3 overall. Female predominance was specifically noted within the patient population (Table 3).
T2DM patients were evaluated for thyroid function across various durations of their diabetes. It was found that the incidence of subclinical hypothyroidism raised as the duration of diabetes increased. Overt hypothyroidism and euthyroid sick syndrome were more frequently seen in individuals with diabetes lasting longer than 5 years. Overall, thyroid dysfunction of any type was significantly more prevalent in patients with T2DM lasting longer than 5 years. Subclinical hypothyroidism was the most commonly observed condition across all duration groups (Table 5).
The scatter plot depicts the interrelationship between HbA1c (A biomarker for long-term glycemic control) and TSH (A biomarker of thyroid function) in 100 individuals diagnosed with T2DM. A discernible positive correlation is evident between HbA1c percentages and TSH concentrations (µIU/mL). As elevated HbA1c values signify inadequate glycemic control, TSH levels generally demonstrate a corresponding increase, suggesting a likely link between suboptimal glycemic control and thyroid dysfunction. Notably, a statistically robust positive association (r = 0.76, p < 0.001) was established linking elevated TSH levels with poor glycemic control (HbA1c > 8%) (Figure 2).
The thyroid status of all T2DM patients was assessed based on gender. A female predominance in overall thyroid dysfunction was identified across the entire patient cohort. A statistically significant relationship was noted between thyroid function and gender (Chi-square [χ²] = 10.2, p = 0.03), with the prevalence of hypothyroidism being higher among females. Specifically, subclinical hypothyroidism represented the most frequent thyroid abnormality observed in females diagnosed with T2DM (Figure 3).
Discussion
The current study demonstrated thyroid dysfunction in T2DM patients, with subclinical hypothyroidism identified as the most prevalent form (24%). In contrast, the non-diabetic cohort exhibited a minimal prevalence of thyroid disorders. These findings align with prior research, which has established a significantly increased risk of thyroid dysfunction among diabetic individuals (1-4). The high frequency of subclinical hypothyroidism specifically underscores a strong clinical link between T2DM and altered thyroid function, supporting established literature and emphasizing the need for routine thyroid screening in all diabetic patients (7-16).
In individuals with long-term T2DM, a greater frequency of both overt hypothyroidism and euthyroid sick syndrome was observed, indicating progressive endocrine-metabolic dysregulation associated with the chronic nature of the disease. The prevalence of thyroid dysfunction demonstrated a direct relationship with the duration of T2DM. This elevated incidence of hypothyroidism is consistent with progressive dysregulation, underscoring the necessity of screening thyroid hormone levels in patients with long-standing T2DM (13,14). Persistent hyperglycemia and insulin resistance are known to compromise the function of the hypothalamic-pituitary axis. Elevated plasma glucose concentrations potentially inhibit the hypothalamic release of thyrotropin-releasing hormone (TRH). This action disrupts the normal feedback loop, which could then lead to increased TSH levels through an effect on hypothalamic neurons. This mechanism may also reduce sensitivity to circulating thyroid hormones. Prior research supports this hypothesis, demonstrating both disrupted circadian TSH secretion and altered TRH-TSH axis responsiveness in patients with uncontrolled T2DM. Insulin and its associated downstream signaling cascade elements are principally situated within the cortical and hippocampal brain regions. Key molecular components implicated in compromised insulin signaling encompass the insulin receptor substrate (IRS), phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), and glycogen synthase kinase-3 beta (GSK-3β). The aberrant functioning of these core molecules, whether through enhanced or reduced phosphorylation-leading to activation or inactivation-is central to the development of insulin signaling defects or insulin resistance (3-15).
Significantly higher TSH concentrations demonstrated a strong positive correlation with suboptimal glycemic control, specifically measured by HbA1c (r = 0.76, p < 0.001). This observed association suggests that deteriorating glucose regulation relates to either an increased incidence or greater severity of thyroid gland impairment, notably subclinical or overt hypothyroidism. Such thyroid dysfunction could potentially exacerbate insulin resistance or, alternatively, manifest as a result of chronic metabolic stress, thereby confirming its likely contribution to the worsening of insulin resistance (10,11). Persistent hyperglycemia triggers a cascade involving oxidative stress, the release of cytokines, and microvascular injury within endocrine organs, including the thyroid gland. The resulting accumulation of advanced glycation end-products (AGEs) in thyroid tissue, along with concurrent local inflammation, may disrupt TSH receptor signaling or the process of iodide uptake. This ultimately compromises thyrocyte function, culminating in the development of hypothyroidism and elevated levels of TSH (17-19).
Thyroid dysfunction was observed more frequently among female patients, particularly those who were postmenopausal, and in individuals suffering from diabetes for longer than 5 years. This highlights the critical necessity for proactive screening for thyroid dysfunction, specifically targeting postmenopausal women and patients with chronic diabetes (12,13).
Conclusion
A considerable proportion of T2DM patients present with undiagnosed thyroid dysfunction, which can negatively affect their glycemic control. Crucially, the prevalent subclinical thyroid dysfunction should not be overlooked; regular screening is essential to mitigate diabetes-related complications and achieve optimal glycemic control. A significant number of individuals with long-standing diabetes who fail to meet their glycemic targets, despite sufficient therapeutic intervention, are often found to exhibit abnormal TSH concentrations. Diabetic women experiencing menopause frequently and asymptomatically exhibit elevated serum TSH levels. These observations collectively underscore the imperative for TSH screening both during the initial diagnostic workup and throughout the annual follow-up of all T2DM individuals. It is therefore recommended to develop innovative, risk-stratified protocols for thyroid screening in T2DM. These protocols should consider specific high-risk factors: Female post-menopausal status, a history of chronically poor glycemic control (HbA1c > 8%), and a longer duration of T2DM (> 5 years). This approach will enable earlier detection and foster improved integrated endocrine management. A limitation of the current research is its inability to fully characterize the etiology of thyroid dysfunction among T2DM patients, a factor that could directly impact their metabolic status. Furthermore, to effectively establish thyroid screening protocols within T2DM management, there is a clear requirement for meta-analyses and longitudinal, multi-center studies. These efforts are necessary to validate the efficacy of specific biochemical parameter ranges-such as HbA1c thresholds indicating poor glycemic control-alongside gender, age, and duration of T2DM.
Acknowledgement
I would like to thank the faculty members of the Department of Biochemistry and the Department of Pharmacology, as well as to all the technical personnel at Government Medical College (GMC), Anantapur, India. Their invaluable support, expert guidance, constructive critique, and assistance were instrumental in the successful completion of this research endeavor.
Funding sources
None.
Ethical statement
This study received formal approval from the Institutional Ethics Committee of GMC Anantapuramu, Andhra Pradesh, India (Project code: 10-D/2021), which was sanctioned on October 1st, 2021. Prior to their involvement, informed consent was meticulously obtained from all participants before they were officially enrolled in the study.
Conflicts of interest
No conflict of interest.
Author contributions
Dr. Sadiya Sanjer: Major contributor to data collection, interpretation of patient data results, and drawing all final conclusions regarding the prevalence and patterns of thyroid dysfunction in T2DM. Dr. SN Bhagyamma: Overall proofreading and collecting relevant literature. Dr. Mohammed Abdul Majeed: Supporting in all aspects, including excluding patients on drugs influencing thyroid, statistical tools, and organizing data into tables and figures. All authors have read and approved the final manuscript.
Data availability statement
All data is confidential and safely maintained on a drive by the authors.
Full-Text: (37 Views)
Introduction
Type 2 diabetes mellitus (T2DM) and thyroid dysfunction constitute significant endocrine disorders, sharing intricate clinical and metabolic overlaps. The systemic concentrations of circulating thyroid hormones influence various organs and cellular functions via nuclear receptor mechanisms. Specifically, thyroid hormones exert considerable control over the homeostasis of glucose, lipid, and protein metabolism. The thyroid, a key endocrine gland, is susceptible to compromise due to persistent states of hyperglycemia and the body’s ongoing compensatory mechanisms aimed at addressing this chronic carbohydrate dysregulation. Multiple research studies have consistently documented minor fluctuations in the concentrations of thyroid hormones within individuals with diabetes (1-3). While the co-occurrence of T2DM and thyroid dysfunction might be coincidental, specific pathological links exist, involving conditions such as polyglandular autoimmune syndromes 1 and 2, multiple endocrine neoplasia (MEN) types 1 and 3, and various genetic or autoimmune factors. Although numerous etiologies underlie thyroid dysfunction, it is significant that hyperthyroidism actively detrimentally affects glycemic control in diabetic patients, whereas subclinical hypothyroidism shows a strong association with impaired blood glucose control and heightened cardiovascular risk. The clinical importance of thyroid disorders in diabetic patients becomes much greater when thyroid function is impaired, as this can result in severe complications, such as frequent hypoglycemia in hypothyroidism and potentially life-threatening ketoacidosis in thyrotoxicosis, making diabetes management more challenging (4-6). While routine screening for dyslipidemia and nephropathy is common in T2DM, thyroid screening is not consistently prioritized. Therefore, diabetic patients should undergo annual thyroid screening to identify any asymptomatic thyroid dysfunction (7).
The current research is designed to assess the frequency and characteristic distribution of thyroid hormone alterations among individuals with T2DM. It will also examine the relationship between these alterations and glycemic control (Glycated hemoglobin [HbA1c), the duration of T2DM, and the patient's age and gender. Furthermore, the study aims to underscore the imperative for routine thyroid screening within T2DM management, proposing stratified protocols essential for comprehensive, integrated endocrine care.
Methods
This observational, cross-sectional study was implemented over a 12-month period at a tertiary care teaching hospital in India. Prior to commencement, Institutional Ethics Committee approval was secured, and informed consent was obtained from all recruited participants. The study ultimately encompassed a total of 200 subjects. This cohort comprised two equally sized groups: A patient group, consisting of 100 diagnosed T2DM cases, aged 30 to 70 years and of both genders, and a control group, consisting of 100 non-diabetic individuals meticulously matched for both age and gender. A comprehensive clinical history was recorded, and participants underwent a thorough physical examination and complete biochemical evaluation. Individuals reporting a prior diagnosis of thyroid disease, those taking thyroid-altering medications, and pregnant women were systematically excluded. The final dataset was collected and organized to include demographic variables (Age and gender), the duration of T2DM, and specific biochemical parameters, including fasting blood sugar (FBS), postprandial blood sugar (PPBS), HbA1c, thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4). Anti-thyroid peroxidase (TPO) testing, although optional, was not performed because our study aimed to assess thyroid status and determine the necessity for treatment, rather than investigate the causes of thyroid dysfunction. Standard reference ranges were used to interpret the various biochemical parameters (Table 1) (8-10).
Type 2 diabetes mellitus (T2DM) and thyroid dysfunction constitute significant endocrine disorders, sharing intricate clinical and metabolic overlaps. The systemic concentrations of circulating thyroid hormones influence various organs and cellular functions via nuclear receptor mechanisms. Specifically, thyroid hormones exert considerable control over the homeostasis of glucose, lipid, and protein metabolism. The thyroid, a key endocrine gland, is susceptible to compromise due to persistent states of hyperglycemia and the body’s ongoing compensatory mechanisms aimed at addressing this chronic carbohydrate dysregulation. Multiple research studies have consistently documented minor fluctuations in the concentrations of thyroid hormones within individuals with diabetes (1-3). While the co-occurrence of T2DM and thyroid dysfunction might be coincidental, specific pathological links exist, involving conditions such as polyglandular autoimmune syndromes 1 and 2, multiple endocrine neoplasia (MEN) types 1 and 3, and various genetic or autoimmune factors. Although numerous etiologies underlie thyroid dysfunction, it is significant that hyperthyroidism actively detrimentally affects glycemic control in diabetic patients, whereas subclinical hypothyroidism shows a strong association with impaired blood glucose control and heightened cardiovascular risk. The clinical importance of thyroid disorders in diabetic patients becomes much greater when thyroid function is impaired, as this can result in severe complications, such as frequent hypoglycemia in hypothyroidism and potentially life-threatening ketoacidosis in thyrotoxicosis, making diabetes management more challenging (4-6). While routine screening for dyslipidemia and nephropathy is common in T2DM, thyroid screening is not consistently prioritized. Therefore, diabetic patients should undergo annual thyroid screening to identify any asymptomatic thyroid dysfunction (7).
The current research is designed to assess the frequency and characteristic distribution of thyroid hormone alterations among individuals with T2DM. It will also examine the relationship between these alterations and glycemic control (Glycated hemoglobin [HbA1c), the duration of T2DM, and the patient's age and gender. Furthermore, the study aims to underscore the imperative for routine thyroid screening within T2DM management, proposing stratified protocols essential for comprehensive, integrated endocrine care.
Methods
This observational, cross-sectional study was implemented over a 12-month period at a tertiary care teaching hospital in India. Prior to commencement, Institutional Ethics Committee approval was secured, and informed consent was obtained from all recruited participants. The study ultimately encompassed a total of 200 subjects. This cohort comprised two equally sized groups: A patient group, consisting of 100 diagnosed T2DM cases, aged 30 to 70 years and of both genders, and a control group, consisting of 100 non-diabetic individuals meticulously matched for both age and gender. A comprehensive clinical history was recorded, and participants underwent a thorough physical examination and complete biochemical evaluation. Individuals reporting a prior diagnosis of thyroid disease, those taking thyroid-altering medications, and pregnant women were systematically excluded. The final dataset was collected and organized to include demographic variables (Age and gender), the duration of T2DM, and specific biochemical parameters, including fasting blood sugar (FBS), postprandial blood sugar (PPBS), HbA1c, thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4). Anti-thyroid peroxidase (TPO) testing, although optional, was not performed because our study aimed to assess thyroid status and determine the necessity for treatment, rather than investigate the causes of thyroid dysfunction. Standard reference ranges were used to interpret the various biochemical parameters (Table 1) (8-10).
|
Table 1. Standard reference values for biochemical parameters
.PNG) FBS: Fasting Blood Sugar, PPBS: Postprandial Blood Sugar, HbA1c: Glycated Hemoglobin, TSH: Thyroid Stimulating Hormone, FT3: Free Triiodothyronine, FT4: Free Thyroxine |
|
Table 2. Thyroid status classification
.PNG) TSH: Thyroid Stimulating Hormone, FT3: Free Triiodothyronine, FT4: Free Thyroxine |
Data analysis was conducted using SPSS software version 25.0. Continuous variables were reported as the mean ± standard deviation, while categorical variables were presented as percentages. Statistical relationships were assessed using Pearson's correlation for continuous data and the chi-square (χ²) test for categorical data.
Results
The study cohort comprised 58% female and 42% male participants (Mean age = 52.4 ± 10.2 years), with a mean duration of T2DM exceeding 7 years (7.1 ± 3.5 years). T2DM patients demonstrated an elevated mean HbA1c value of 8.2 ± 1.3 overall. Female predominance was specifically noted within the patient population (Table 3).
|
Table 3. Patient demographics
.PNG) T2DM: Type 2 Diabetes Mellitus, HbA1c: Glycated Hemoglobin |
|
Table 4. Prevalence of thyroid dysfunction in type 2 diabetes mellitus (T2DM)
.PNG) |
T2DM patients were evaluated for thyroid function across various durations of their diabetes. It was found that the incidence of subclinical hypothyroidism raised as the duration of diabetes increased. Overt hypothyroidism and euthyroid sick syndrome were more frequently seen in individuals with diabetes lasting longer than 5 years. Overall, thyroid dysfunction of any type was significantly more prevalent in patients with T2DM lasting longer than 5 years. Subclinical hypothyroidism was the most commonly observed condition across all duration groups (Table 5).
The scatter plot depicts the interrelationship between HbA1c (A biomarker for long-term glycemic control) and TSH (A biomarker of thyroid function) in 100 individuals diagnosed with T2DM. A discernible positive correlation is evident between HbA1c percentages and TSH concentrations (µIU/mL). As elevated HbA1c values signify inadequate glycemic control, TSH levels generally demonstrate a corresponding increase, suggesting a likely link between suboptimal glycemic control and thyroid dysfunction. Notably, a statistically robust positive association (r = 0.76, p < 0.001) was established linking elevated TSH levels with poor glycemic control (HbA1c > 8%) (Figure 2).
The thyroid status of all T2DM patients was assessed based on gender. A female predominance in overall thyroid dysfunction was identified across the entire patient cohort. A statistically significant relationship was noted between thyroid function and gender (Chi-square [χ²] = 10.2, p = 0.03), with the prevalence of hypothyroidism being higher among females. Specifically, subclinical hypothyroidism represented the most frequent thyroid abnormality observed in females diagnosed with T2DM (Figure 3).
.PNG) Figure 1. Thyroid dysfunction in type 2 diabetes mellitus (T2DM) patients versus controls Table 5. Duration of type 2 diabetes mellitus (T2DM) versus thyroid dysfunction status in type 2 diabetes mellitus (T2DM) patients .PNG) T2DM: Type 2 Diabetes Mellitus .PNG) Figure 2. Correlation between glycated hemoglobin (HbA1c) and thyroid stimulating hormone (TSH) levels in type 2 diabetes mellitus patients |
.PNG) Figure 3. Gender-wise thyroid dysfunction in type 2 diabetes mellitus (T2DM) |
Discussion
The current study demonstrated thyroid dysfunction in T2DM patients, with subclinical hypothyroidism identified as the most prevalent form (24%). In contrast, the non-diabetic cohort exhibited a minimal prevalence of thyroid disorders. These findings align with prior research, which has established a significantly increased risk of thyroid dysfunction among diabetic individuals (1-4). The high frequency of subclinical hypothyroidism specifically underscores a strong clinical link between T2DM and altered thyroid function, supporting established literature and emphasizing the need for routine thyroid screening in all diabetic patients (7-16).
In individuals with long-term T2DM, a greater frequency of both overt hypothyroidism and euthyroid sick syndrome was observed, indicating progressive endocrine-metabolic dysregulation associated with the chronic nature of the disease. The prevalence of thyroid dysfunction demonstrated a direct relationship with the duration of T2DM. This elevated incidence of hypothyroidism is consistent with progressive dysregulation, underscoring the necessity of screening thyroid hormone levels in patients with long-standing T2DM (13,14). Persistent hyperglycemia and insulin resistance are known to compromise the function of the hypothalamic-pituitary axis. Elevated plasma glucose concentrations potentially inhibit the hypothalamic release of thyrotropin-releasing hormone (TRH). This action disrupts the normal feedback loop, which could then lead to increased TSH levels through an effect on hypothalamic neurons. This mechanism may also reduce sensitivity to circulating thyroid hormones. Prior research supports this hypothesis, demonstrating both disrupted circadian TSH secretion and altered TRH-TSH axis responsiveness in patients with uncontrolled T2DM. Insulin and its associated downstream signaling cascade elements are principally situated within the cortical and hippocampal brain regions. Key molecular components implicated in compromised insulin signaling encompass the insulin receptor substrate (IRS), phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), and glycogen synthase kinase-3 beta (GSK-3β). The aberrant functioning of these core molecules, whether through enhanced or reduced phosphorylation-leading to activation or inactivation-is central to the development of insulin signaling defects or insulin resistance (3-15).
Significantly higher TSH concentrations demonstrated a strong positive correlation with suboptimal glycemic control, specifically measured by HbA1c (r = 0.76, p < 0.001). This observed association suggests that deteriorating glucose regulation relates to either an increased incidence or greater severity of thyroid gland impairment, notably subclinical or overt hypothyroidism. Such thyroid dysfunction could potentially exacerbate insulin resistance or, alternatively, manifest as a result of chronic metabolic stress, thereby confirming its likely contribution to the worsening of insulin resistance (10,11). Persistent hyperglycemia triggers a cascade involving oxidative stress, the release of cytokines, and microvascular injury within endocrine organs, including the thyroid gland. The resulting accumulation of advanced glycation end-products (AGEs) in thyroid tissue, along with concurrent local inflammation, may disrupt TSH receptor signaling or the process of iodide uptake. This ultimately compromises thyrocyte function, culminating in the development of hypothyroidism and elevated levels of TSH (17-19).
Thyroid dysfunction was observed more frequently among female patients, particularly those who were postmenopausal, and in individuals suffering from diabetes for longer than 5 years. This highlights the critical necessity for proactive screening for thyroid dysfunction, specifically targeting postmenopausal women and patients with chronic diabetes (12,13).
Conclusion
A considerable proportion of T2DM patients present with undiagnosed thyroid dysfunction, which can negatively affect their glycemic control. Crucially, the prevalent subclinical thyroid dysfunction should not be overlooked; regular screening is essential to mitigate diabetes-related complications and achieve optimal glycemic control. A significant number of individuals with long-standing diabetes who fail to meet their glycemic targets, despite sufficient therapeutic intervention, are often found to exhibit abnormal TSH concentrations. Diabetic women experiencing menopause frequently and asymptomatically exhibit elevated serum TSH levels. These observations collectively underscore the imperative for TSH screening both during the initial diagnostic workup and throughout the annual follow-up of all T2DM individuals. It is therefore recommended to develop innovative, risk-stratified protocols for thyroid screening in T2DM. These protocols should consider specific high-risk factors: Female post-menopausal status, a history of chronically poor glycemic control (HbA1c > 8%), and a longer duration of T2DM (> 5 years). This approach will enable earlier detection and foster improved integrated endocrine management. A limitation of the current research is its inability to fully characterize the etiology of thyroid dysfunction among T2DM patients, a factor that could directly impact their metabolic status. Furthermore, to effectively establish thyroid screening protocols within T2DM management, there is a clear requirement for meta-analyses and longitudinal, multi-center studies. These efforts are necessary to validate the efficacy of specific biochemical parameter ranges-such as HbA1c thresholds indicating poor glycemic control-alongside gender, age, and duration of T2DM.
Acknowledgement
I would like to thank the faculty members of the Department of Biochemistry and the Department of Pharmacology, as well as to all the technical personnel at Government Medical College (GMC), Anantapur, India. Their invaluable support, expert guidance, constructive critique, and assistance were instrumental in the successful completion of this research endeavor.
Funding sources
None.
Ethical statement
This study received formal approval from the Institutional Ethics Committee of GMC Anantapuramu, Andhra Pradesh, India (Project code: 10-D/2021), which was sanctioned on October 1st, 2021. Prior to their involvement, informed consent was meticulously obtained from all participants before they were officially enrolled in the study.
Conflicts of interest
No conflict of interest.
Author contributions
Dr. Sadiya Sanjer: Major contributor to data collection, interpretation of patient data results, and drawing all final conclusions regarding the prevalence and patterns of thyroid dysfunction in T2DM. Dr. SN Bhagyamma: Overall proofreading and collecting relevant literature. Dr. Mohammed Abdul Majeed: Supporting in all aspects, including excluding patients on drugs influencing thyroid, statistical tools, and organizing data into tables and figures. All authors have read and approved the final manuscript.
Data availability statement
All data is confidential and safely maintained on a drive by the authors.
Article Type: Research |
Subject:
Biochemistry
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