Association of serum paraoxonase activity with insulin sensitivity and oxidative stress in hyperthyroid and TSH‐suppressed nodular goitre patients

Yavuz, Dilek Gogas; Yüksel, Meral; Deyneli, Oğuzhan; Ozen, Yesim; Aydın, Hasan; Akalın, Sema

doi:10.1111/j.1365-2265.2004.02123.x

Cited by 61 publications

(55 citation statements)

References 28 publications

(51 reference statements)

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“…Increased HOMA and decreased Matsuda and Belfiore indices in HR and SHR patients compared with euthyroid subjects suggest that insulin resistance is present in both fasting and post-glucose state. Our results are in agreement with those of Yavuz et al (7,8) reporting significantly lower insulin sensitivity in a group of SHR. Interestingly, recent studies have shown that even subtle decreases in the levels of thyroid hormones within the physiological range negatively correlate with the HOMA index (16).…”

Section: Discussionsupporting

confidence: 83%

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Studies of insulin resistance in patients with clinical and subclinical hyperthyroidism

Maratou

Hadjidakis

Peppa

et al. 2010

European Journal of Endocrinology

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Objective: Although clinical hyperthyroidism (HR) is associated with insulin resistance, the information on insulin action in subclinical hyperthyroidism (SHR) is limited. Design and methods: To investigate this, we assessed the sensitivity of glucose metabolism to insulin in vivo (by an oral glucose tolerance test) and in vitro (by measuring insulin-stimulated rates of glucose transport in isolated monocytes) in 12 euthyroid subjects (EU), 16 patients with HR, and 10 patients with SHR. Results: HR and SHR patients displayed higher postprandial glucose levels (area under the curve, AUC 0-300 32 190G1067 and 31 497G716 mg/dl min respectively) versus EU (27 119 G1156 mg/dl min, P!0.05). HR but not SHR patients displayed higher postprandial insulin levels (AUC 0-300 11 020G985 and 9565G904 mU/l min respectively) compared with EU subjects (AUC 0-300 7588G743 mU/l min, P!0.05). Homeostasis model assessment index was increased in HR and SHR patients (2.81G0.3 and 2.43G0.38 respectively) compared with EU subjects (1.27 G0.16, P!0.05), while Matsuda and Belfiore indices were decreased in HR (4.21G0.41 and 0.77G0.05 respectively, P!0.001) and SHR patients (4.47G0.33 and 0.85G0.05 respectively, P!0.05 versus EU (7.76G0.87 and 1 respectively). At 100 mU/ml insulin, i) GLUT3 levels on the monocyte plasma membrane were increased in HR (468.8G7 mean fluorescence intensity (MFI)) and SHR patients (522.2G25 MFI) compared with EU subjects (407G18 MFI, P!0.01 and P!0.05 respectively), ii) glucose transport rates in monocytes (increases from baseline) were decreased in HR patients (37.8G5%) versus EU subjects (61.26G10%, P!0.05). Conclusions: Insulin-stimulated glucose transport in isolated monocytes of patients with HR was decreased compared with EU subjects. Insulin resistance was comparable in patients with both HR and SHR.

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Section: Discussionsupporting

confidence: 83%

“…The studies in the literature regarding insulin resistance in SHR are scarce and controversial. Insulin sensitivity in patients with iatrogenic SHR has been reported to be either reduced (7,8) or unaltered (9).…”

Section: Introductionmentioning

confidence: 99%

Studies of insulin resistance in patients with clinical and subclinical hyperthyroidism

Maratou

Hadjidakis

Peppa

et al. 2010

European Journal of Endocrinology

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“…Among the studies conducted to date, those regarding insulin resistance in SHR are few and their results are controversial. Adamczyk et al only observed a weak impairment of insulin sensitivity that was associated with the lower activity of plasma paraoxonase [9,19]. Other authors, in their papers on iatrogenic SHR, describe a lower or unchanged level of insulin sensitivity.…”

Section: Hyperthyroidismmentioning

confidence: 99%

Insulinooporność a choroby tarczycy

Gierach¹,

Gierach²,

Junik³

2014

Endokrynologia Polska

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Insulin resistance is defined as a glucose homeostasis disorder involving a decreased sensitivity of muscles, adipose tissue, liver and other body tissues to insulin, despite its normal or increased concentration in blood. Insulin resistance may be asymptomatic or occur presenting a variety of disorders, such as: glucose tolerance impairment, type 2 diabetes, as well as hypercholesterolaemia, hypertriglyceridaemia, obesity, and arterial hypertension. Insulin acts via specific receptors present on the surface of most cells of the body. The greatest number of these receptors is found on adipocytes, hepatocytes and striated muscle cells. There are three mechanisms of insulin resistance: pre-receptor, receptor and post-receptor. Multiple methods of assessing insulin resistance are based on the concurrent measurements of glucose and insulin levels in blood serum. The glucose and insulin measurements are conducted in baseline conditions or after intravenous administration of a specific quantity of glucose or insulin. The methods of assessing insulin resistance are divided into direct and indirect. The current 'gold standard' in the assessment of insulin sensitivity is the determination of tissue glucose utilisation using the metabolic clamp technique. The presence of disorders of carbohydrate metabolism has been demonstrated in thyroid disease involving either overt hyperthyroidism or overt hypothyroidism. The severity of the disease is proportional to the severity of these disorders. The possible influence of subclinical forms of both hyperthyroidism and hypothyroidism on carbohydrate disorders is still under discussion. Thyroid hormones have a significant effect on glucose metabolism and the development of insulin resistance. In hyperthyroidism, impaired glucose tolerance may be the result of mainly hepatic insulin resistance, whereas in hypothyroidism the available data suggests that the insulin resistance of peripheral tissues prevails. StreszczenieInsulinooporność definiuje się jako zaburzenie homeostazy glukozy polegające na zmniejszonej wrażliwości mięśni, tkanki tłuszczowej, wątroby oraz innych tkanek na insulinę pomimo jej prawidłowego lub podwyższonego stężenia we krwi. Insulinooporność może przebiegać bezobjawowo lub towarzyszyć różnorodnym chorobom i zaburzeniom, takim jak upośledzona tolerancja glukozy, cukrzyca typu 2, hipercholesterolemia, hipertriglicerydemia, otyłość i nadciśnienie tętnicze. Insulina działa za pośrednictwem swoistych receptorów obecnych na powierzchni większości komórek organizmu. Najwięcej tych receptorów stwierdza się na komórkach tłuszczowych, hepatocytach i komórkach mięśni poprzecznie prążkowanych. Wyróżnia się trzy rodzaje insulinooporności: przedreceptorową, receptorową i poreceptorową. Metody rozpoznawania insulinooporności oparte są na jednoczesnym oznaczaniu stężenia glukozy i insuliny w surowicy krwi. Pomiary stężenia glukozy i insuliny wykonywane są albo w warunkach podstawowych, albo po dożylnym podaniu określonej ilości glukozy lub insuliny. Metody oceny insulin...

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“…2A), the resident macrophages of the liver (29,39). In man, hyperthyroidism is characterized by significant changes in circulating parameters related to oxidative stress, including (i) higher levels of lipid peroxidation indicators (40)(41)(42)(43)(44)(45)(46)(47)(48)(49); (ii) enhancement in hydrogen peroxide and lipid hydroperoxide levels (49); and (iii) diminished levels of antioxidants such as a-tocopherol (41), coenzyme Q (44), ascorbic acid (41), and reduced thiols (42,46,50). These changes correlated with the enhancement in urinary lipid peroxidation products (40) and chemiluminescence response (51) and are either significantly reduced or normalized by thyrostatic therapy or antioxidant supplementation (40-46, 49, 50).…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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SummaryThyroid hormone (L-3,3 0 ,5-triiodothyronine, T 3 ) exerts calorigenic effects by accelerating mitochondrial O 2 consumption through transcriptional activation of respiratory genes, with consequent increased reactive oxygen species (ROS) production. In the liver, ROS generation occurs at different sites of hepatocytes and in the respiratory burst of Kupffer cells, triggering the activation of the transcription factors nuclear factor-jB, signal transducer and activator of transcription 3, and activating protein 1. Under these conditions, the redox upregulation of Kupffer cell-dependent expression of cytokines [tumor necrosis factor-a, interleukin (IL)-1, and IL-6] is achieved, which upon interaction with specific receptors in hepatocytes trigger the expression of antioxidant enzymes (manganese superoxide dismutase, inducible nitric oxide synthase), antiapoptotic proteins (Bcl-2), and acute-phase proteins (haptoglobin, b-fibrinogen). These responses and the promotion of hepatocyte and Kupffer cell proliferation observed represent hormetic effects re-establishing redox homeostasis, promoting cell survival, and protecting the liver against ischemia-reperfusion (IR) injury. It is proposed that hormesis underlying T 3 action may constitute a novel preconditioning strategy for IR injury during liver surgery in man or in liver transplantation using reduced-size grafts from living donors, considering that (i) with the exception of the controversial ischemic preconditioning, all other studied strategies have failed to reach the clinical setting and (ii) T 3 is a well-tolerated therapeutic agent that either lacks major adverse effects or has minimal and controlled side effects. IUBMBIUBMB Life, 62(6): [460][461][462][463][464][465][466] 2010

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Association of serum paraoxonase activity with insulin sensitivity and oxidative stress in hyperthyroid and TSH‐suppressed nodular goitre patients

Cited by 61 publications

References 28 publications

Studies of insulin resistance in patients with clinical and subclinical hyperthyroidism

Studies of insulin resistance in patients with clinical and subclinical hyperthyroidism

Insulinooporność a choroby tarczycy

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

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