Association of hyperthyroidism with serum leptin levels

Nakamura, Tomoatsu; Nagasaka, Shoichiro; Ishikawa, San‐e; Hayashi, Hiroko; Saitô, Takako; Kusaka, Ikuyo; Higashiyama, Minori; Saito, Toshikazu

doi:10.1053/meta.2000.9520

Cited by 19 publications

(18 citation statements)

References 24 publications

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“…Based on the studies summarized in the previous section there is not enough evidence for a relationship between autoimmune thyroid disease and leptin. None of the studies found any correlation between serum leptin and thyroid autoantibodies, and four of the studies found evidence that thyroid function is more important than autoimmunity in determining serum leptin concentrations (78,81,84,88).…”

Section: Leptin and Thyroid Autoimmunitymentioning

confidence: 92%

Circulating leptin and thyroid dysfunction

Zimmermann-Belsing

Brabant²,

Holst³

et al. 2003

Eur J Endocrinol

153

111

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The identification and sequencing of the ob gene and its product, leptin, in 1994 opened new insights in the study of the mechanisms controlling body weight and led to a surge of research activity. Since its discovery, leptin has been the subject of an enormous amount of work especially within the fields of nutrition, metabolism and endocrinology. Leptin is accepted as an adipose signal, and even though the underlying mechanisms are not fully clarified, leptin, in addition to the thyroid hormones, is believed to be involved in regulation during the switch from the fed to the starved state. It is not clear whether leptin and the melanocortin pathways interact with the thyroid axis under physiological conditions other than during starvation or in response to severe illness, both states in which the hypothalamo -pituitary -thyroid axis may be severely suppressed. In addition to the suggested central relationship between leptin and thyroid hormones, there might also be a peripheral relationship although this effect is not clear. Both thyroid hormones and leptin might be involved in the adaptive thermogenesis through mitochondrial uncoupling proteins and heat production because both thyroxine and triiodothyronine are involved in the starvation-induced decrease in thermogenesis. Both rodent and human studies of leptin have failed to show any consistent relationship between thyroid function and serum leptin concentrations. However, leptin might have an important role in thyroid pathophysiology due to thyroid hormone involvement in thermogenesis and regulation of uncoupling proteins. In this review, we have focused on leptin in relation to thyroid pathophysiology.

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Section: Leptin and Thyroid Autoimmunitymentioning

confidence: 92%

Circulating leptin and thyroid dysfunction

Zimmermann-Belsing

Brabant²,

Holst³

et al. 2003

Eur J Endocrinol

153

111

View full text Add to dashboard Cite

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“…Numerous studies of human serum leptin concentration during abnormal thyroid function have shown conflicting results (Corbetta et al, 1997;Diekman et al, 1998;Leonhardt et al, 1998;Ozata et al, 1998;Pinkney et al, 1998;Sesmilo et al, 1998;Zimmermann-Belsing et al, 1998;Miyakawa et al, 1999;Chen et al, 2000;Nakamura et al, 2000;Obermayer-Pietsch et al, 2001;Wahrenberg et al, 2002). Some data indicate that hyperthyroidism in man increases serum leptin concentration (Diekman et al, 1998;Ozata et al, 1998;Chen et al, 2000;Nakamura et al, 2000), while other data show that it decreases (Pinkney et al, 1998;ZimmermannBelsing et al, 1998;Miyakawa et al, 1999;Obermayer-Pietsch et al, 2001), or does not affect (Corbetta et al, 1997;Wahrenberg et al, 2002) serum leptin concentration. Hypothyroidism has been shown to increase (Leonhardt et al, 1998;Sesmilo et al, 1998;Chen et al, 2000), or decrease (Diekman et al, 1998) serum leptin levels, or to leave them unaffected (Corbetta et al, 1997;Ozata et al, 1998;Sesmilo et al, 1998;Miyakawa et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…Hypothyroidism has been shown to increase (Leonhardt et al, 1998;Sesmilo et al, 1998;Chen et al, 2000), or decrease (Diekman et al, 1998) serum leptin levels, or to leave them unaffected (Corbetta et al, 1997;Ozata et al, 1998;Sesmilo et al, 1998;Miyakawa et al, 1999). The lack of T 3 effect on leptin secretion by human adipocytes (Menendez et al, 2001) is difficult to explain in the light of some in vivo studies indicating that hyperthyroidism affected serum leptin concentration (Diekman et al, 1998;Ozata et al, 1998;Pinkney et al, 1998;Zimmermann-Belsing et al, 1998;Miyakawa et al, 1999;Chen et al, 2000;Nakamura et al, 2000;Obermayer-Pietsch et al, 2001). It has been reported that T 3 up-regulates leptin gene expression in 3T3-L1 adipocytes (Yoshida et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Evidence that triiodothyronine decreases rat serum leptin concentration by down-regulation of leptin gene expression in white adipose tissue

2006

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“…14 Treatment of healthy volunteers with T 3 led to hyperthyroid metabolic indices, but no change in serum leptin levels. 11 If some studies did not find different leptin levels among euthyroid, hyperthyroid and hypothyroid individuals, 10,15 other studies found increased leptin levels in subjects with moderate hyperthyroidism 16 or lower leptin levels in hypothyroidism. 9 Recently, Kok et al 17 reported a direct relationship between 24-h levels of thyrotropic hormone (TSH) and 24-h levels of leptin in moderately obese women.…”

Section: Introductionmentioning

confidence: 99%

Daylong pituitary hormones in morbid obesity: effects of bariatric surgery

et al. 2008

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Moderate obesity is known to be associated with multiple endocrine abnormalities. Less information is available on the hormonal status of patients with morbid obesity and on the effects of major weight loss. We studied 16 severely obese (BMI 40.6-69.9 kg/m 2 ) nondiabetic patients and 7 nonobese (BMI range 24.6-27.7 kg/m 2 ), sex-and age-matched healthy volunteers. During 24 h in a metabolic ward, four meals were administered and hourly blood samples were drawn from a central venous catheter for the measurement of glucose, insulin, leptin, thyrotropic hormone (TSH), growth hormone (GH) and prolactin. Insulin sensitivity was measured by a euglycaemic hyperinsulinaemic clamp. Studies were repeated 6 months after biliopancreatic diversion, a mainly malabsorptive surgical approach, which caused an average weight loss of 35±4 kg (or 26 ± 2% of initial weight). Compared with controls, patients were hyperinsulinaemic (290 ± 31 vs 88 ± 4 pmol l À1 , P ¼ 0.0002), insulin resistant (23.5±2.8 vs 52.9±4.9 mmol min À1 kg FFM À1 , P ¼ 0.0006) and hyperleptinaemic (52.5±5.8 vs 10.9±3 ng ml À1 , P ¼ 0.0002). Plasma TSH levels were increased throughout the day-night cycle (averaging 2.02 ± 0.18 vs 1.09 ± 0.19 mU ml À1 of controls, P ¼ 0.01), whereas serum GH levels were suppressed (0.46±0.10 vs 3.01±1.15, P ¼ 0.002). Following surgery, the hyperinsulinaemia and insulin resistance were fully normalized; in concomitance with a major drop in leptin levels (to 14.4±2.7 ng ml À1 , P ¼ 0.02), TSH decreased and GH increased to near-normal levels. In the whole dataset, mean 24-h leptin levels were directly related to mean 24-h TSH levels after controlling for confounders this relationship was lost only after adjusting for fat mass. We conclude that in morbid obesity leptin is a determinant of changes in pituitary function.

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Association of hyperthyroidism with serum leptin levels

Cited by 19 publications

References 24 publications

Circulating leptin and thyroid dysfunction

Circulating leptin and thyroid dysfunction

Evidence that triiodothyronine decreases rat serum leptin concentration by down-regulation of leptin gene expression in white adipose tissue

Daylong pituitary hormones in morbid obesity: effects of bariatric surgery

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