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ORIGINAL ARTICLE
Year : 2020  |  Volume : 9  |  Issue : 9  |  Page : 4637-4640  

Idiopathic post prandial glucose lowering, a whistle blower for subclinical hypothyroidism and insulin resistance. A cross-sectional study in Tertiary Care Centre of northeast India


1 Department of Biochemistry, Neigrihms, Shillong-18, Meghalaya, India
2 Department of Medicine, Neigrihms, Shillong-18, Meghalaya, India
3 Department of Community Medicine, Neigrihms, Shillong-18, Meghalaya, India
4 Department of Physiology, Neigrihms, Shillong-18, Meghalaya, India

Date of Submission15-May-2020
Date of Decision14-Jun-2020
Date of Acceptance07-Jul-2020
Date of Web Publication30-Sep-2020

Correspondence Address:
Dr. Chandan Kr Nath
Department of Biochemistry, Neigrihms, Shillong-18, Meghalaya
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jfmpc.jfmpc_867_20

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  Abstract 


Background and Aims: There has been a lot of confusion in management of apparently healthy individuals whose post prandial plasma glucose levels were lower than fasting levels. It has been observed that many clinicians do send for repeat tests to rule out analytical error since there is common knowledge that post prandial glucose should be higher than fasting glucose level. Blood glucose level is regulated by a fully integrated mechanism with complex interplay of hormones and enzymes on metabolic pathways. Increase or decrease of thyroid hormones can break this equilibrium leading to alterations of carbohydrate metabolism. The objective for this study was to look for subclinical hypothyroidism (SCH) and insulin resistance (IR) in Idiopathic Post prandial glucose lowering and the correlation between thyroid stimulating hormone (TSH) with IR in them. Methods: A cross-sectional study with subgroup analysis, 34 cases and 34 controls. Cases comprises of otherwise healthy individuals whose post prandial glucose is lower than fasting glucose and controls as those healthy individual whose post prandial glucose is higher than fasting. Thyroid hormones and insulin were measured in fasting serum samples. Homeostasis model assessment for IR was calculated as per formula. Results: Among the 34 cases with idiopathic post prandial glucose lowering, 76% (n = 26) had subclinical hypothyroidism and 61% (n = 21) had insulin resistance. A positive correlation (r = 0.55) was observed between Thyroid-Stimulating hormone (TSH) and Index of insulin resistance and homeostatic model assessment (HOMA-IR) and was statistically significant with P < 0.1. Conclusions: The study highlights the importance of evaluating glycoregulatory hormones like thyroid hormones and insulin in cases with idiopathic post prandial glucose lowering for early diagnosis and prevention of overt clinical diseases like Hypothyroidism and Diabetes Mellitus.

Keywords: Idiopathic post prandial glucose lowering, insulin resistance, subclinical hypothyroidism, thyroid stimulating hormone


How to cite this article:
Longkumer C, Nath CK, Barman B, Ruram AA, Visi V, Yasir M D, Sangma MA. Idiopathic post prandial glucose lowering, a whistle blower for subclinical hypothyroidism and insulin resistance. A cross-sectional study in Tertiary Care Centre of northeast India. J Family Med Prim Care 2020;9:4637-40

How to cite this URL:
Longkumer C, Nath CK, Barman B, Ruram AA, Visi V, Yasir M D, Sangma MA. Idiopathic post prandial glucose lowering, a whistle blower for subclinical hypothyroidism and insulin resistance. A cross-sectional study in Tertiary Care Centre of northeast India. J Family Med Prim Care [serial online] 2020 [cited 2020 Oct 21];9:4637-40. Available from: https://www.jfmpc.com/text.asp?2020/9/9/4637/296359




  Introduction Top


Studies have reported that some apparently healthy individuals showed lower post prandial plasma glucose levels than fasting levels.[1],[2] There has been a lot of confusion in management of these apparently healthy individuals whose post prandial plasma glucose levels were lower than fasting levels. It has been observed that many clinicians do send for repeat tests to rule out analytical error since there is common knowledge that post prandial glucose should be higher than fasting glucose level. Blood glucose level is regulated by a fully integrated mechanism with complex interplay of hormones and enzymes on key metabolic pathways.[3] An intimate relationship between thyroid hormones and carbohydrate metabolism has long been established. Influence of thyroid hormones on insulin action to different organs can be both agonistic and antagonistic, however, maintaining a fine balance between these opposing actions is required for normal glucose metabolism. An increase or decrease of thyroid hormones can break this balance leading to alterations of carbohydrate metabolism.[4],[5] Recently, increased interest has focused on the association between thyroid dysfunction and obesity, diabetes, metabolic syndrome and other cardiovascular risk factors[6],[7],[8] Previous studies have established overt hypothyroidism as a risk factor for insulin resistance (IR).[9] Subclinical hypothyroidism (SCH) often goes unrecognized due to lack of signs and symptoms.[10] Various studies have suggested the possible adverse clinical outcomes of subclinical hypothyroidism, including cardiac dysfunction, dyslipidaemia leading to an increased risk of atherosclerosis, and neuropsychiatric symptoms. Several more recent meta-analyses of observational studies found an association between SCH and coronary artery disease.[11] There are various studies of post prandial glucose lowering and various hormonal counter regulatory response to hypoglycaemia[1],[3] but sparse study on whether idiopathic post prandial glucose lowering is related to thyroid dysfunction and insulin resistance.

In the light of these reports, this study was conducted to find out if post prandial glucose lowering is a whistle blower indicating some subclinical conditions. Once the correlation is determined, it should be aimed to correct the disorder, or if that is not possible, to attain measures to reduce and treat it before development of overt clinical disorder or complication.


  Methods Top


This hospital-based study was started after obtaining clearance from NEIGRIHMS Scientific Advisory Committee (NSAC) and Institute Ethics Committee (IEC) 2/07/2019. A cross sectional design with subgroup analysis, 34 cases and 34 controls, were enrolled prospectively from outpatient department of General Medicine Department of our hospital within a time period of 8 months between July 2019 -February 2020. Cases comprises of otherwise healthy individual whose post prandial glucose is lower than fasting glucose and healthy individual whose post prandial glucose is higher than fasting, were taken as control.

Inclusion criteria

  1. Adults (18-60 years) whose fasting blood glucose >post prandial blood glucose in otherwise normal individual with no prior history of Diabetes Mellitus or Impaired Fasting Glucose or Impaired Glucose tolerance
  2. Willingness to participate in the study.


Exclusion criteria

  1. Strenuous exercise
  2. Smoking
  3. Known case of Diabetes Mellitus, hypothyroidism, hyperinsulinemia, adrenocortical hypofunction, decreased gastrointestinal absorption like sprue and coeliac disease
  4. Medication: oral hypoglycemic drugs, anti- diabetic, anti-inflammatory drugs.


About 5ml of fasting blood sample was drawn from all subjects after an overnight fast, also after 2 hours post prandial. The serum was separated by centrifuging the blood at 3000 rpm for 10 minutes. Serum glucose and lipid profile levels was estimated by spectrophotometric method. (AU2700 Chemistry auto-analyser, Beckman Coulter, Inc.), while serum FT3, FT4, TSH, and Insulin were measured by Chemiluminescence immunoassay method (UniCel DxI 800, Beckman Coulter, Inc.).

Insulin resistance was estimated using following calculated parameters:

Homeostatic model assessment in assessing insulin resistance (HOMA-IR) = [Fasting glucose (mg/dl) * fasting insulin (micro IU/ml)]/405.

Patient were considered as insulin resistant when HOMA-IR ≥ 1.4.[12]

And diagnosed to have subclinical hypothyroidism when their free triiodothyronine (FT3) and free thyroxine (FT4) were normal, but thyroid stimulating hormone (TSH) was >4 mU/I.[13]

Statistical analysis

Database was constructed in Microsoft Excel 2007, and statistical analysis was done using IBM Statistical Package for the Social Sciences (SPSS) MacOS version 23 (SPSS Inc., Illinois, USA), t-test and Pearson's correlation test were done to analyse the data. P < 0.05 was considered statistically significant.


  Results Top


In this study, there were in total 68 participants, which was sub-grouped into 34 cases and 34 controls.

[Table 1]: This table shows that majority of cases were in age group 31-40 years (44.1%). Also more than half of the cases (64.7%) were females.
Table 1: Age and sex distribution of the study group/respondents

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[Table 2]: This table shows that that out of the 34 cases, 76% (n = 26) had subclinical hypothyroidism (SCH) and 61% (n = 21) had insulin resistance (HOMA-IR).
Table 2: Prevalence of the subclinical hypothyroidism and insulin resistance by study group

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  Discussion Top


Glucose is an essential fuel for the brain, therefore, adequate uptake of glucose from the plasma is key for normal brain function and survival. Despite wide variations in glucose flux (i.e. fed state, fasting state, etc), blood glucose is maintained in a very narrow range. This is accomplished by a series of hormonal and physiologic responses. As a result, hypoglycaemia is a rare occurrence in normal individuals.[3] It is well understood how this glucose counter-regulatory responses are altered in patients with diabetes, but this is not the case in a healthy normal individual. In this regard, keeping in mind the various interplay of hormones in glucose metabolism, in our study we found that out of the 34 cases, 76% (n = 26) had subclinical hypothyroidism (SCH) and 61% (n = 21) had insulin resistance (HOMA-IR) [Table 2]. A positive correlation (r = 0.55) was observed between TSH and HOMA IR and was statistically significant with P < 0.01[Figure 1]. This is in accordance with the study done by Maratou E et al.[14], AL Sayed et al.[15]
Figure 1: Correlation test was done between TSH and HOMA-IR among the cases and was found to be positively associated (r = 0.55) and significant at 0.01 level

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The maximum prevalence of cases was seen in age group 31-40 years (44.1% of cases) and more common in women than in men (64.7%, n = 22) [Table 1]. This is in accordance with study done by AL Sayed et al.[15] and BM Singh.[16]

Elevated LDL cholesterol, total cholesterol level, and triglycerides has been widely used to assess lipid atherogenesis and Insulin resistance. Thyroid disease can also increase the risk of cardiovascular disease. In the present study, we found a significantly higher proportion of total cholesterol and LDL cholesterol levels among cases [Table 3], which is an important risk factor for cardiovascular disorders.[11],[17],[18]
Table 3: Mean with standard deviation (SD) in case and control groups

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It is not clear as to whether SCH is related to risk for cardiovascular disease (CVD), although it has been concluded recently that mild thyroid failure is associated with an increased risk for development of atherosclerosis[19] and that SCH is a strong indicator for risk of atherosclerosis and myocardial infarction in women.[15]

Continuous exposure to a plethora of cardiovascular risk factors including hyperinsulinemia, dyslipidaemia and undetected SCH may lead to overt and complicated metabolic disease.

Therefore, there is a need for routine assay of thyroid hormones and Insulin resistance in patients with idiopathic post prandial glucose lowering so as to diagnose subclinical disorders as early as possible and reduce morbidity and prevent them from overt clinical disorder like Diabetes, Hypothyroidism and related complications.


  Conclusion Top


The results of the studies we conducted on the 34 cases and 34 controls clearly highlights the importance of evaluating glycoregulatory hormones like thyroid hormones and insulin in cases with idiopathic post prandial glucose lowering. This is especially true for early diagnosis and prevention of overt clinical diseases like Hypothyroidism and Diabetes Mellitus.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Saha B. Post prandial plasma glucose level less than the fasting level in otherwise healthy individuals during routine screening. Indian J Clin Biochem 2006;21:67-71.  Back to cited text no. 1
    
2.
Stuart K, Field A, Raju J, Ramachandran S. Postprandial reactive hypoglycaemia: Varying presentation patterns on extended glucose tolerance tests and possible therapeutic approaches. Case Rep Med 2013;2013:1-5.  Back to cited text no. 2
    
3.
Sprague JE, Arbeláez AM. Glucose counterregulatory responses to hypoglycemia. Pediatr Endocrinol 2013;9:463-75.  Back to cited text no. 3
    
4.
Roubsanthisuk W, Watanakejorn P, Tunlakit M, Sriussadaporn S. Hyperthyroidism induces glucose intolerance by lowering both insulin secretion and peripheral insulin sensitivity. J Med Assoc Thail 2006;89:133-40.  Back to cited text no. 4
    
5.
Kim MK, Kwon HS, Baek KH, Lee JH, Park WC, Sohn HS,et al. Effects of thyroid hormone on A1C and glycated albumin levels in nondiabetic subjects with overt hypothyroidism. Diabetes Care 2010;33:2546-8.  Back to cited text no. 5
    
6.
Iwen KA, Schröder E, Brabant G. Thyroid hormones and the metabolic syndrome. Eur Thyroid J 2013;2:83-92.  Back to cited text no. 6
    
7.
Teixeira PFDS, Dos Santos PB, Pazos-Moura CC. The role of thyroid hormone in metabolism and metabolic syndrome. Ther Adv Endocrinol Metab 2020;11:2042018820917869.  Back to cited text no. 7
    
8.
Biondi B, Kahaly GJ, Robertson RP. Thyroid dysfunction and diabetes mellitus: Two closely associated disorders. Endocr Rev 2019;40:789-824.  Back to cited text no. 8
    
9.
Vyakaranam S, Vanaparthy S, Nori S, Palarapu S, Bhongir AV. Study of insulin resistance in subclinical hypothyroidism. Int J Health Sci Res 2014;4:147-53.  Back to cited text no. 9
    
10.
Mendes D, Alves C, Silverio N, Marques FB. Prevalence of undiagnosed hypothyroidism in Europe: A systematic review and meta-analysis. Eur Thyroid J 2019;8:130-43  Back to cited text no. 10
    
11.
Rodondi N, Aujesky D, Vittinghoff E, Cornuz J, Bauer DC. Subclinical hypothyroidism and the risk of coronary heart disease: A meta-analysis. Am J Med 2006;119:541-51.  Back to cited text no. 11
    
12.
Lee CH, Shih AZ, Woo YC, Fong CH, Leung OY, Janus E, et al. Optimal cut-offs of homeostasis model assessment of insulin resistance (HOMA-IR) to identify dysglycemia and type 2 diabetes mellitus: A 15-year prospective study in Chinese. PLoS One 2016;11:e0163424.  Back to cited text no. 12
    
13.
Cojić M, Cvejanov-Kezunović L. Subclinical hypothyroidism – whether and when to start treatment ? Open Access Maced J Med Sci 2017;5:1042-6.  Back to cited text no. 13
    
14.
Maratou E, Hadjidakis DJ, Kollias A, Tsegka K, Peppa M, Alevizaki M, et al. Studies of insulin resistance in patients with clinical and subclinical hypothyroidism. Eur J Endocrinol 2009;160:785-90.  Back to cited text no. 14
    
15.
Al Sayed A, Al Ali N, Bo Abbas Y, Alfadhli E. Subclinical hypothyroidism is associated with early insulin resistance in Kuwaiti women. Endocr J 2006;53:653-7.  Back to cited text no. 15
    
16.
Singh BM, Goswami B, Mallika V. Association between insulin resistance and hypothyroidism in females attending a tertiary care hospital. Indian J Clin Biochem 2010;25:141-5.  Back to cited text no. 16
    
17.
Irace C, Carallo C, Scavelli FB, De Franceschi MS, Esposito T, Tripolino C, et al. Markers of insulin resistance and carotid atherosclerosis. A comparison of the homeostasis model assessment and triglyceride glucose index. Int J Clin Pract 2013;67:665-72.  Back to cited text no. 17
    
18.
Gayoum AA A. The Effect of Hypothyroidism on Insulin Sensitivity and Their Influence on the Serum Lipid Profile and Renal Function. Endocrinol Metab Syndr. 2016;5(5);1-5.  Back to cited text no. 18
    
19.
McDermott MT, Ridgway EC. Subclinical hypothyroidism is mild thyroid failure and should be treated. J Clin Endocrinol Metab 2001;86:4585-90.  Back to cited text no. 19
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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