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Links between Thyroid Disorders and Glucose Homeostasis
Young Sil Eom, Jessica R. Wilson, Victor J. Bernet
Diabetes Metab J. 2022;46(2):239-256.   Published online March 24, 2022
DOI: https://doi.org/10.4093/dmj.2022.0013
  • 11,536 View
  • 656 Download
  • 24 Web of Science
  • 21 Crossref
AbstractAbstract PDFPubReader   ePub   
Thyroid disorders and diabetes mellitus often coexist and are closely related. Several studies have shown a higher prevalence of thyroid disorders in patients with diabetes mellitus and vice versa. Thyroid hormone affects glucose homeostasis by impacting pancreatic β-cell development and glucose metabolism through several organs such as the liver, gastrointestinal tract, pancreas, adipose tissue, skeletal muscles, and the central nervous system. The present review discusses the effect of thyroid hormone on glucose homeostasis. We also review the relationship between thyroid disease and diabetes mellitus: type 1, type 2, and gestational diabetes, as well as guidelines for screening thyroid function with each disorder. Finally, we provide an overview of the effects of antidiabetic drugs on thyroid hormone and thyroid disorders.

Citations

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    Nutrients.2023; 15(3): 600.     CrossRef
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  • The Correlation Between Thyroid Parameters and the Ratios of Neutrophil/Lymphocyte and Platelet/Lymphocyte in Euthyroid Type 2 Diabetic Patients
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Others
Mitochondrial Toxins and Healthy Lifestyle Meet at the Crossroad of Hormesis
Yu-Mi Lee, Duk-Hee Lee
Diabetes Metab J. 2019;43(5):568-577.   Published online October 24, 2019
DOI: https://doi.org/10.4093/dmj.2019.0143
  • 6,064 View
  • 94 Download
  • 11 Web of Science
  • 11 Crossref
AbstractAbstract PDFPubReader   

Mitochondrial function is crucial for the maintenance of cellular homeostasis under physiological and stress conditions. Thus, chronic exposure to environmental chemicals that affect mitochondrial function can have harmful effects on humans. We argue that the concept of hormesis should be revisited to explain the non-linear responses to mitochondrial toxins at a low-dose range and develop practical methods to protect humans from the negative effects of mitochondrial toxins. Of the most concern to humans are lipophilic chemical mixtures and heavy metals, owing to their physical properties. Even though these chemicals tend to demonstrate no safe level in humans, a non-linear dose-response has been also observed. Stress response activation, i.e., hormesis, can explain this non-linearity. Recently, hormesis has reemerged as a unifying concept because diverse stressors can induce similar stress responses. Besides potentially harmful environmental chemicals, healthy lifestyle interventions such as exercise, calorie restriction (especially glucose), cognitive stimulation, and phytochemical intake also activate stress responses. This conceptual link can lead to the development of practical methods that counterbalance the harm of mitochondrial toxins. Unlike chemical hormesis with its safety issues, the activation of stress responses via lifestyle modification can be safely used to combat the negative effects of mitochondrial toxins.

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Original Article
Others
Comparison of the Usefulness of the Updated Homeostasis Model Assessment (HOMA2) with the Original HOMA1 in the Prediction of Type 2 Diabetes Mellitus in Koreans
Young Seok Song, You-Cheol Hwang, Hong-Yup Ahn, Cheol-Young Park
Diabetes Metab J. 2016;40(4):318-325.   Published online May 27, 2016
DOI: https://doi.org/10.4093/dmj.2016.40.4.318
  • 4,546 View
  • 84 Download
  • 40 Web of Science
  • 42 Crossref
AbstractAbstract PDFPubReader   
Background

The original homeostasis model assessment (HOMA1) and the updated HOMA model (HOMA2) have been used to evaluate insulin resistance (IR) and β-cell function, but little is known about the usefulness of HOMA2 for the prediction of diabetes in Koreans. The aim of this study was to demonstrate the usefulness of HOMA2 as a predictor of type 2 diabetes mellitus in Koreans without diabetes.

Methods

The study population consisted of 104,694 Koreans enrolled at a health checkup program and followed up from 2001 to 2012. Participants were divided into a normal glucose tolerance (NGT) group and a pre-diabetes group according to fasting glucose and glycosylated hemoglobin levels. Anthropometric and laboratory data were measured at the baseline checkup, and HOMA values were calculated at the baseline and follow-up checkups. The hazard ratios (HRs) of the HOMA1 and HOMA2 values and the prevalence of diabetes at follow-up were evaluated using a multivariable Cox proportional hazards model and Kaplan-Meier analysis.

Results

After adjusting for several diabetes risk factors, all of the HOMA values except 1/HOMA1-β and 1/HOMA2-β in the NGT group were significant predictors of the progression to diabetes. In the NGT group, there was no significant difference in HOMA1-IR (HR, 1.09; 95% confidence interval [CI], 1.04 to 1.14) and HOMA2-IR (HR, 1.11; 95% CI, 1.04 to 1.19). However, in the pre-diabetes group, 1/HOMA2-β was a more powerful marker (HR, 1.29; 95% CI, 1.26 to 1.31) than HOMA1-IR (HR, 1.23; 95% CI, 1.19 to 1.28) or 1/HOMA1-β (HR, 1.14; 95% CI, 1.12 to 1.16). In the non-diabetic group (NGT+pre-diabetes), 1/HOMA2-β was also a stronger predictor of diabetes (HR, 1.27; 95% CI, 1.25 to 1.29) than HOMA1-IR (HR, 1.14; 95% CI, 1.12 to 1.15) or 1/HOMA1-β (HR, 1.13; 95% CI, 1.11 to 1.14).

Conclusion

HOMA2 is more predictive than HOMA1 for the progression to diabetes in pre-diabetes or non-diabetic Koreans.

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Reviews
Ubiquitin Ligases in Cholesterol Metabolism
Wei Jiang, Bao-Liang Song
Diabetes Metab J. 2014;38(3):171-180.   Published online June 17, 2014
DOI: https://doi.org/10.4093/dmj.2014.38.3.171
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AbstractAbstract PDFPubReader   

To maintain cholesterol homeostasis, the processes of cholesterol metabolism are regulated at multiple levels including transcription, translation, and enzymatic activity. Recently, the regulation of protein stability of some key players in cholesterol metabolism has been characterized. More and more ubiquitin ligases have been identified including gp78, Hrd1, TRC8, TEB4, Fbw7, and inducible degrader of low density lipoprotein receptor. Their working mechanisms and physiological functions are becoming revealed. Here, we summarize the structure, substrates and function of these ubiquitin ligases. Their potential application in drug discovery is also discussed.

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Periodontitis and Insulin Resistance: Casual or Causal Relationship?
Abhijit N. Gurav
Diabetes Metab J. 2012;36(6):404-411.   Published online December 12, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.6.404
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AbstractAbstract PDFPubReader   

Insulin resistance (IR) is now considered as a chronic and low level inflammatory condition. It is closely related to altered glucose tolerance, hypertriglyceridemia, abdominal obesity, and coronary heart disease. IR is accompanied by the increase in the levels of inflammatory cytokines like interleukin-1 and 6, tumor necrosis factor-α. These inflammatory cytokines also play a crucial part in pathogenesis and progression of insulin resistance. Periodontitis is the commonest of oral diseases, affecting tooth investing tissues. Pro-inflammatory cytokines are released in the disease process of periodontitis. Periodontitis can be attributed with exacerbation of IR. Data in the literature supports a "two way relationship" between diabetes and periodontitis. Periodontitis is asymptomatic in the initial stages of disease process and it often escapes diagnosis. This review presents the blurred nexus between periodontitis and IR, underlining the pathophysiology of the insidious link. The knowledge of the association between periodontitis and IR can be valuable in planning effectual treatment modalities for subjects with altered glucose homeostasis and diabetics. Presently, the studies supporting this association are miniscule. Further studies are mandatory to substantiate the role of periodontitis in the deterioration of IR.

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Original Articles
Analysis of the Relative Importance of Insulin Resistance and Insulin Secretion Defect by Homeostasis Model Assessment in Korean Type 2 Diabetic Patients.
Wan Sub Shim, Soo Kyung Kim, Hae Jin Kim, Jae Hoon Moon, Eun Seok Kang, Yu Mie Rhee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2005;29(3):206-214.   Published online May 1, 2005
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is characterized by defects in both insulin secretion and insulin sensitivity. However, the relative importance of insulin secretion and insulin resistance in Korean type 2 diabetic patients has not been well characterized in any study that has included a large number of subjects. Therefore, this study aimed to evaluate the relative importance of insulin sensitivity and the function of the beta cell in Korean type 2 diabetic patients. METHODS: We applied the HOMA model to 1,162 type 2 diabetic patients (654 males and, 508 females) who did not use insulin and we assessed HOMAIR and HOMAbetacell & its relation to the other parameters. RESULTS: The HOMAIR of Korean type 2 diabetic patients was 2.29(range: 0.31~37.17) and the HOMAbetacell of Korean type 2 diabetic patients was 32.17(range: 1.04~1310.79). The HOMAIR of Korean type 2 diabetic male patients was 2.15(range: 0.31~16.6) and that of Korean type 2 diabetic female patients was 2.47(range: 0.36~37.17). The HOMAbetacell of Korean type 2 diabetic male patients was 30.1(range: 1.04~462.34) and that of Korean type 2 diabetic female patients was 35.42(range: 2.60~1310.79). The HOMAIR and HOMAbetacell were significantly higher in females than males. There was no significant correlation between HOMAIR and age, and the duration of diabetes, but there was significant correlation between HOMAIR and BMI, fasting glucose, HbA1c and the fasting insulin. There was no significant correlation between age and HOMAbetacell. However, there was significant correlation between HOMAbetacell and BMI, the duration of diabetes, the fasting glucose, HbA1c and the fasting insulin. The longer the duration of diabetes, the more the HOMAbetacell was decreased but there was no change of HOMAIR with respect to the duration of diabetes. As expected, the subjects with a lower HOMAIR and a higher HOMAbetacell had the best glycemic control. Those with a higher HOMAIR and lower HOMAbetacell had the worst glycemic control although they had taken larger amount of oral hypoglycemic agents. Interestingly, the patients with a lower HOMAIR and higher HOMAbetacell had better glycemic control than those patients with a higher HOMAIR and lower HOMAbetacell. CONCLUSION: Both insulin secretion and insulin resistance are important in glycemic control but it seems that insulin secretion is a more important factor in glycemic control than insulin resistance in the Korean type 2 diabetic patients
Limitation of Validity of Homeostasis Model Assessment as a Index of Insulin Resistance.
Yong Seok Yun, Seok Won Park, Young Duk Song, Hyo Kyung Park, Oh Yoen Kim, Chul Woo Ahn, Jae Hyun Nam, Su Youn Nam, Bong Soo Cha, Chong Ho Lee, Sumg Gil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
Korean Diabetes J. 2000;24(5):541-551.   Published online January 1, 2001
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AbstractAbstract
BACKGROUND
Homeostasis model assessment of insulin resistance (HOMAIR) had been proposed as a simple and inexpensive alternative to other complex procedures measuring insulin resistance. We evaluated the validity of HOMAIR, comparing to total glucose disposal rate measured by euglycemic clamp test in 63 subjects with normal glucose tolerance, 21 with impaired glucose tolerance and 47 with type 2 DM. METHODS: HOMAIR and HOMA cell function (Homeostasis model assessment of cell function) were calculated with formula described by Matthews [HOMAIR: fasting insulin ( U/mL) X fasting glucose (mmol/L) / 22.5, HOMA cell function: 20 X fasting insulin ( U/mL) / (fasting glucose (mmol/L) - 3.5)]. 2-hour euglycemic (5 mmol/L) hyper insulinemic (717 pmol/L) clamp test were carried out. RESULTS: The strong inverse correlation (r=-0.658, <0.001) was shown between log transformed HOMAIR and total glucose disposal rates. The agreement of two methodes in the categorization according to insulin resistance was moderate (weighed kappa=0.45). The magnitude of correlation coefficients were smaller in subjects with lower BMI (BMI < 23.7 kg/m2, r = -0.441 vs BMI > or = 23.7 kg/m2, r = -0.693, p = 0.0183), lower HOMA cell function (HOMA cell function < 57.2, r = -0.514 vs HOMA cell function > or = 57.2, r = -0.773, p = 0.0091) and higher fasting glucose levels (fasting glucose < 102 mg/dL, r = -0.697 vs fasting glucose > or = 102 mg/dL, r = -0.59, p = 0.0735). The results of correlation analysis was not significant in diabetics with lower BMI. CONCLUSION: Limitation of validity of HOMAIR should be carefully considered in subjects with lower BMI and lower fasting insulin to glucose levels, such as lean type 2 diabetes with insulin secretory defects.

Diabetes Metab J : Diabetes & Metabolism Journal