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German Centre for Cardiovascular Research (DZHK), partner site Greifswald, Greifswald, Germany
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German Centre for Cardiovascular Research (DZHK), partner site Greifswald, Greifswald, Germany
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Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany
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Charité – Universitätsmedizin Berlin, BCRT – Berlin Institute of Health Center for Regenerative Therapies, Berlin, Germany
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Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany
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intolerance and heightened insulin resistance ( 2 , 3 ). The effects of hypothyroidism on glucose metabolism appear to be complex and even puzzling since clinical findings point into seemingly contrasting directions: on the one hand, hypothyroidism is
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Introduction Hypothyroidism, either subclinical or overt, has been associated with increased risk of coronary artery disease [ 1 , 2 , 3 ]. It is also known to be associated with insulin resistance [ 4 ] and dyslipidemia [ 5 ] characterized by
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individuals with TSH values exceeding 7.0 mIU/l, and particularly above 10 mIU/l [ 6 ]. In spite of this controversy, some studies have linked SCH with hypertension [ 7 ], obesity [ 8 ], dyslipidemia [ 9 ], metabolic syndrome [ 10 ], insulin resistance [ 10
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abnormal glucose tolerance and diabetes mellitus have been reported to occur in a significant proportion of patients with hyperthyroidism [ 2 ]. Several factors like changes in insulin resistance, beta-cell function, abnormal gastric emptying, and
Laboratorio 6, Departamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados-Instituto Politécnico Nacional, Delegación Tlalpan, Ciudad de México, México
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to obtain the survival percentage. Determination of glucose tolerance and insulin resistance Tests were performed at the beginning of week 40 as 1 per day, after 6 h of fasting. For the insulin resistance test, each animal received 0.75 IU
Department of Medicine, Thyroid Outpatient Clinic, Division of Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo, Sao Paulo, Brazil
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Lipid Clinic Heart Institute (InCor), University of Sao Paulo Medical School Hospital, Sao Paulo, Brazil
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School of Medicine, Faculdade Israelita de Ciências da Saúde Albert Einstein, Sao Paulo, Brazil
Center for Clinical and Epidemiological Research, University Hospital, University of São Paulo School of Medicine, Sao Paulo, Brazil
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Introduction Thyroid hormones are involved in the regulation of body composition, lipid metabolism, and insulin resistance [ 1 - 6 ]. It is well known that hypothyroidism is associated with high levels of LDL-cholesterol and triglycerides
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metabolic effects when used as a pharmacological agent in animal studies. Administered to hypothyroid rats, 3,5-T 2 prevented and even reversed the severe consequences typically induced by a high-fat diet, like weight gain, insulin resistance or hepatic
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Department of Endocrinology, The Christie Manchester Academic Health Science Centre, Manchester, UK
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insulin resistance as an essential causative factor, has been defined as the presence of visceral obesity with at least two of the following disorders: (1) raised triglyceride level or specific treatment, (2) reduced HDL cholesterol or specific treatment
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Department of Diabetes and Endocrinology, Skåne University Hospital, Malmö, Sweden
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Department of Ophthalmology, Skåne University Hospital, Malmö, Sweden
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Department of Diabetes and Endocrinology, Skåne University Hospital, Malmö, Sweden
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supported by the association of the Thr92Ala SNP with psychological well-being and response to T3 or T4 treatment [ 11 ]. SNPs in DIO2 have been associated with obesity, insulin resistance, and type 2 diabetes [ 12 - 16 ]; however, some studies could not
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Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
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disrupted [ 38 ]. In contrast, other studies showed that higher serum TSH and lower serum FT4 levels were associated with increased insulin resistance markers [ 39 , 40 ] and elevated blood glucose levels [ 41 ], due to contribution of pathological pathways