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      A Low Free T3 to Free T4 Ratio Is Associated with Sarcopenia in Euthyroid Patients with Type 2 Diabetes Mellitus

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          Abstract

          Background

          This research evaluated the link between normal thyroid hormone levels and sarcopenia in patients with type 2 diabetes mellitus (T2DM).

          Methods

          This cross-sectional study enrolled 312 euthyroid patients with T2DM from Qilu Hospital of the Shandong University, China. Body composition, grip strength, and physical performance were assessed as per the 2019 consensus guidelines of the Asian Working Group for Sarcopenia. Binary logistic regression was used to examine the correlation between thyroid hormone levels and sarcopenia and its components.

          Results

          The prevalence of sarcopenia was 26.9%. Following adjustments for potential confounders, a high-normal serum free triiodothyronine (FT3) level (odds ratio (OR) = 0.522, 95% confidence interval (CI): 0.304–0.895, P = 0.018), a low-normal serum free thyroxine (FT4) level (OR = 1.126, 95% CI: 1.009–1.258, P = 0.034), and a heightened FT3/FT4 ratio (OR = 0.923, 95% CI: 0.879–0.969, P = 0.001) were linked to a low prevalence of sarcopenia. Considering the components of sarcopenia, FT3 concentration was positively associated with muscle strength (OR = 0.525, 95% CI: 0.305–0.902, P = 0.020) and physical performance (OR = 0.443, 95% CI: 0.259–0.758, P = 0.003), while FT4 concentration was negatively linked to muscle mass (OR = 1.114, 95% CI: 1.009–1.232, P = 0.036). The FT3/FT4 ratio was positively linked to muscle mass (OR = 0.943, 95% CI: 0.905–0.981, P = 0.006), muscle strength (OR = 0.945, 95% CI: 0.901–0.992, P = 0.021), and physical performance (OR = 0.934, 95% CI: 0.894–0.975, P = 0.002). Nevertheless, thyroid-stimulating hormone concentration was not associated with sarcopenia.

          Conclusion

          A high FT3/FT4 ratio was significantly linked to a lowered risk of sarcopenia in euthyroid patients with T2DM.

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          Most cited references48

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          Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

          D. Matthews, J Hosker, A Rudenski … (1985)
          The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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            Asian Working Group for Sarcopenia: 2019 Consensus Update on Sarcopenia Diagnosis and Treatment

            Liang-Kung Chen, Jean Woo, Prasert Assantachai … (2020)
            Clinical and research interest in sarcopenia has burgeoned internationally, Asia included. The Asian Working Group for Sarcopenia (AWGS) 2014 consensus defined sarcopenia as "age-related loss of muscle mass, plus low muscle strength, and/or low physical performance" and specified cutoffs for each diagnostic component; research in Asia consequently flourished, prompting this update. AWGS 2019 retains the previous definition of sarcopenia but revises the diagnostic algorithm, protocols, and some criteria: low muscle strength is defined as handgrip strength <28 kg for men and <18 kg for women; criteria for low physical performance are 6-m walk <1.0 m/s, Short Physical Performance Battery score ≤9, or 5-time chair stand test ≥12 seconds. AWGS 2019 retains the original cutoffs for height-adjusted muscle mass: dual-energy X-ray absorptiometry, <7.0 kg/m2 in men and <5.4 kg/m2 in women; and bioimpedance, <7.0 kg/m2 in men and <5.7 kg/m2 in women. In addition, the AWGS 2019 update proposes separate algorithms for community vs hospital settings, which both begin by screening either calf circumference (<34 cm in men, <33 cm in women), SARC-F (≥4), or SARC-CalF (≥11), to facilitate earlier identification of people at risk for sarcopenia. Although skeletal muscle strength and mass are both still considered fundamental to a definitive clinical diagnosis, AWGS 2019 also introduces "possible sarcopenia," defined by either low muscle strength or low physical performance only, specifically for use in primary health care or community-based health promotion, to enable earlier lifestyle interventions. Although defining sarcopenia by body mass index-adjusted muscle mass instead of height-adjusted muscle mass may predict adverse outcomes better, more evidence is needed before changing current recommendations. Lifestyle interventions, especially exercise and nutritional supplementation, prevail as mainstays of treatment. Further research is needed to investigate potential long-term benefits of lifestyle interventions, nutritional supplements, or pharmacotherapy for sarcopenia in Asians.
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              Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation.

              K.G.M.M. Alberti, P.Z. Zimmet (1998)
              The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
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                Author and article information

                Contributors
                Lei Gong:
                ORCID: https://orcid.org/0000-0001-8846-6590
                Li Chen:
                ORCID: https://orcid.org/0000-0001-7670-8062
                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date Collection: 2022
                Publication date (Electronic): 17 August 2022
                Volume: 2022
                Electronic Location Identifier: 2305156
                Affiliations
                1Department of Endocrinology, Qilu Hospital of Shandong University, Jinan 250012, China
                2Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan 250012, China
                3Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province Medicine & Health, Jinan 250012, China
                4Jinan Clinical Research Center for Endocrine and Metabolic Diseases, Jinan 250012, China
                Author notes

                Academic Editor: Antonio Brunetti

                Author information
                https://orcid.org/0000-0001-6504-5750
                https://orcid.org/0000-0003-2045-1290
                https://orcid.org/0000-0001-8846-6590
                https://orcid.org/0000-0001-7670-8062
                Article
                DOI: 10.1155/2022/2305156
                PMC ID: 9402295
                PubMed ID: 36034587
                SO-VID: 46c56c4e-bb11-4544-8f97-88ff5af39b90
                Copyright © Copyright © 2022 Kewei Wang et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 5 January 2022
                Date revision received : 16 June 2022
                Date accepted : 3 August 2022
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81873632
                Categories
                Subject: Research Article

                Data availability:

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