Thyroid hormones and lipogenesis from glucose in rat fat cells

The effect of thyroidectomy on lipogenesis from glucose was investigated in rat fat cells. It was shown that thyroidectomy resulted in a clear increase in the oxidation of glucose to CO₂ and also in its conversion to fatty acids. Such an increase in lipogenesis from glucose after thyroidectomy was not due to a change in the cell size or to a modification of the cell surface. The diffusion of L-glucose and the facilitated diffusion transport of 3-0 methyl glucose were not increased; the increase in glucose oxidation observed after thyroidectomy is therefore not the result of an increased transfer of glucose. In contrast, the uptake of deoxyglucosc, a sugar which enters the cell and is phosphorylated by the hexokinase system, but is then not further metabolized, was markedly enhanced in cells from the thyroidectomized animals. A 4–5-fold increase over control in the V_max, but no change in the K_m, were observed. Since no effects were noted on sugar diffusion or transport, this result demonstrates that a major consequence of thyroidectomy is an increase in glucose phosphorylation. Previous observations (Corrèze et al., 1974; Van Inwegen et al., 1975) showed how fat cells from thyroidectomized rats lose their lipolytic capacity; in the present study we provide evidence for an increase in lipogenesis in these same cells. Thyroid hormones might therefore modulate a critical regulatory stcp(s) common to lipolysis and lipogenesis.     

Reduced lipolysis and increased lipogenesis in adipose tissue from pinealectomized rats adapted to training

The current study investigated the effects of chronic training and pinealectomy on the lipogenic and lipolytic activity of adipose tissue. Pinealectomized and sham-operated adult male Wistar rats were distributed in to four subgroups: pinealectomized untrained, pinealectomized trained, control untrained and control trained. At the end of the training period (8 wk) the rats were killed. Blood samples were collected for glucose, insulin and leptin determinations. Peri-epididymal adipocytes were isolated for measurement of in vitro rates of lipolysis and incorporation of substrates (D-[U-14C]-glucose, L-[U-14C]-lactate, [2-14C]-acetate and [1-14C]-palmitate) into lipids, and samples of epididymal adipose tissue were homogenized for evaluation of glucose-6-phosphate dehydrogenase maximal activity. Pinealectomy resulted in a significantly increased lipolytic capacity in response to isoproterenol and a decrease in circulating leptin levels without affecting the rates of incorporation of different substrates into lipids. However, only in the intact control group did training promote a higher basal and isoproterenol-stimulated lipolysis, increase the incorporation of palmitate (esterification), decrease the incorporation of acetate (lipogenesis) into lipids and diminish circulating leptin levels. These effects of exercise training were not seen in pinealectomized rats. However, pinealectomized trained animals showed a marked reduction in lipolysis and an increased rate of acetate incorporation. In conclusion, we demonstrated for the first time that the pineal gland plays an important role in the regulation of lipid metabolism in such a way that its absence caused a severe alteration in the balance between lipogenesis and lipolysis, which becomes evident with the adaptation to exercise training.     

Cyclic AMP and lipogenesis in fat cells from thyroidectomized rats.

Thyroid hormones regulate lipid metabolism by affecting lipogenesis as well as lipolysis. The present paper discusses the way thyroidectomy induced an enhancement in lipogenesis in rat fat cells. The doubling in the conversion of glucose to CO2 and fatty acids seen after thyroidectomy was found to be due to a modification in the actual pathway of glucose metabolism: there was a preferential stimulation of the conversion of glucose to CO2 by the pentose cycle (utilisation of [1-14C]glucose) while the production of fatty acids and glyceride-glycerol proceeded, respectively, much more, or only slightly more, via the pathway of [6-14C]glucose metabolism. Studies employing the phosphodiesterase inhibitor MIX, or the cyclic AMP analogue, DBcAMP showed that the lipogenic process depends on cyclic AMP. As the stimulatory effect of thyroidectomy was not abolished, however, lipogenesis must be under the independent control of both cyclic AMP and absence of thyroid hormones. Insulin, a further mediator of lipogenesis was found to further enhance the already preexisting high conversion of glucose to CO2 in fat cells from thyroidectomized rats. It is concluded that at least three factors modify lipogenesis: thyroidectomy, cyclic AMP and insulin; each achieving its effect in an independent manner.     

β3肾上腺素受体介导的脂解作用与缺血性心衰的关系（英文）

β3肾上腺素受体（β3AR）是新发现的受体,主要参与脂肪组织甘油三酯的降解,产生能量;心衰时心脏中β3AR上调;心肌缺血缺氧时,内源性脂解作用可维持心肌的收缩性;为了维持心功能慢性缺血性心衰代偿期很可能存在能量代谢重建:在神经内分泌激活的同时,以外源性游离脂肪酸（FFA）为主要能量底物,心脏缺血缺氧进一步加重时,β3AR代偿性上调并介导心肌细胞的内源性脂解供能,葡萄糖经由3-磷酸甘油参与合成内源性三酰甘油再脂解而间接供能,葡萄糖的氧化被抑制,此时心肌细胞兼有类似脂肪细胞的功能。心衰时β3AR上调是能量代谢代偿的结果。但上调的β3AR长期过度激活有可能引起心肌组织继发性肉碱缺乏,导致ATP生成障碍使心衰失代偿,因而在心衰失代偿期β3AR阻滞剂可能有利于缓解心衰。而（β3AR激动药最终表现为正性肌力作用还是负性肌力作用,要看在具体的作用部位它对β3AR的直接效应与其对胰岛素的继发效应二者的力量对比）。从理论上讲,β3AR激动药用于慢性缺血性心衰代偿期,既可改善心肌的能量代谢,产生正性肌力作用,又可降低动脉血压,降低心脏的前负荷,从而改善心功能;β3AR激动药还可改善与心衰并存的胰岛素抵抗。心脏能量代谢的缺陷越来越被认为在心衰的进展中起着重要的决定性作用,心脏的代谢适应和适应不良是很有前景的药物治疗新靶点。     

Influence of norepinephrine and exercise on lipolysis in adipose tissue of diabetic rats

Summary The lipolytic effect of norepinephrine (NE) in adipose tissue in vitro was studied before and after exercise in non-fasted rats with severe, untreated streptozotocin diabetes. It was observed that: 1. NE in increasing concentrations stimulated glycerol release in vitro to an equal extent from the adipose tissue of nondiabetic and diabetic rats. However, the re-esterification of free fatty acids (FFA) in adipose tissue in vitro was decreased by NE in diabetic rats as compared to normal rats. 2. During exercise NE further decreased the re-esterification of FFA in vitro in adipose tissue of diabetic rats. 3. Exercise did not change NE-induced glycerol release in vitro in the adipose tissue of diabetic rats. 4. In diabetic animals the increase in plasma glycerol and FFA during exercise was correlated inversely with the NE-induced release of glycerol and FFA from the adipose tissue of the same animals after exercise. The lipolytic effect of NE is not significantly different in adipose tissue of diabetic and nondiabetic rats. By decreasing the re-esterification of FFA in vitro, NE is probably responsible for the observed increase in the release of FFA in vivo, a likely energy source in severely diabetic animals.     

Effect of insulin on glucagon enhanced lipolysis in vitro

Summary Glucagon in concentrations similar to those found in human plasma markedly stimulates lipolysis in rat adipose tissuein vitro. The effects of these physiological concentrations of glucagon are reduced or abolished by insulin at concentrations of 25 and 100U/ml. Considering the marked insulinogenic effect of glucagon these observations may provide an explanation for the delayed increase of blood FFA observed after glucagon injectionin vivo.This work was supported by the Fonds National de la Recherche Scientifique and the Fonds de la Recherche Scientifique Médicale, Belgium.     

Effect of testosterone on lipolysis in human pre-adipocytes from different fat depots

Aim/hypothesis Regional differences in lipolysis, with higher lipolytic activity in visceral than subcutaneous fat, are important for the development of insulin resistance and might be influenced by testosterone.Methods We studied testosterone-regulated lipolysis and protein expression (by western blot) in fully differentiated pre-adipocytes from visceral (omental) and abdominal subcutaneous adipose tissue from 52 human subjects. These cells were isolated and cultured in a serum-free medium.Results Testosterone caused a specific, time- and concentration-dependent 50% reduction of catecholamine-stimulated lipolysis in the subcutaneous depot. Half of the maximum effect occurred at 10 nmol/l. The inhibitory effect was due to the inability of -adrenoceptors and cyclic AMP to stimulate the protein kinase A, hormone-sensitive lipase complex. Testosterone caused a depot-specific 50% reduction of the protein expression of hormone-sensitive lipase and ₂-adrenoceptors in differentiated subcutaneous pre-adipocytes, but no change in ₁-adrenoceptors, protein kinase A subunits or perilipin expression. In contrast, testosterone had no effect on lipolysis or protein expression in the visceral depot. However, testosterone receptors were present in both depots, and the hormone inhibited adipocyte leptin secretion. Similar effects on lipolysis were observed with dihydrotestosterone.Conclusions/interpretation Testosterone in physiological concentrations causes a depot-specific reduction of catecholamine-stimulated lipolysis in subcutaneous fat cells, probably due to reduced protein expression of ₂-adrenoceptors and hormone-sensitive lipase. This could be an important pathogenic factor underlying regional differences in lipolysis and development of insulin resistance and hyperandrogenic polycystic ovary syndrome.Abbreviations PCOS polycystic ovary syndrome - GPDH glycerol-3-phosphate dehydrogenase - AR adrenergic receptor - HSL hormone-sensitive lipase - PKA protein kinase A - OD optical density - dcAMP dibutyryl cyclic AMP     

An abnormality of adrenaline,phentolamine stimulated lipolysis in adipose tissue from obese,maturity-onset diabetics

Summary Abnormalities of fat metabolism fromin vitro andin vivo experiments have elsewhere been described in both diabetes and obesity. In these studies adrenaline (100 M) and phentolamine (100 g/ml) stimulated glycerol release has been compared in adipose tissue from groups of non-diabetic, non-obese, diabetic and obese subjects. Adipose tissue from obese diabetics showed a highly significant (p<0.001) diminution in stimulated lipolysis when compared with non-diabetic, non-obese adipose tissue. The conditions of obesity and diabetes are required to be present simultaneously to maintain this difference in lipolysis. Diabetes or obesity per se are responsible for only marginally significant differences in stimulated glycerol release. The possible reasons for this defect in lipolysis in obese elderly diabetics, pertaining to fat cell receptors, the adenyl cyclase system and the hormone sensitive lipase have been discussed.

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Anomalien bei der durch Adrenalin, Phentolamin stimulierten Lipolyse des Fettgewebes von übergewichtigen Patienten mit spätmanifestem Diabetes

Zusammenfassung Beiin vitro- undin vivo-Studien sind anderweitig sowohl für den Diabetes als auch für die Fettsucht Anomalien des Fettmetabolismus beschrieben worden. In dieser Arbeit wurde die durch Adrenalin (100 M@#@) und Phentolamin (100 g/ml) stimulierte Glycerinfreisetzung im Fettgewebe von Patienten ohne Diabetes, von Patienten ohne Übergewichtigkeit und bei Diabetikern mit Übergewicht miteinander verglichen. Das Fettgewebe von übergewichtigen Diabetikern zeigte eine hochsignifikante (p<0,001) Verminderung der stimulierten Lipolyse im Vergleich zum Fettgewebe von Nicht-Diabetikern und Nicht-Übergewichtigen. Übergewichtigkeit und Diabetes müssen gleichzeitig vorhanden sein, um diesen Unterschied in der Lipolyse aufrecht zu erhalten. Diabetes und Übergewicht allein sind nur für gering signifikante Unterschiede bei der stimulierten Glycerinfreisetzung verantwortlich. Die möglichen Ursachen für diesen Mangel in der Lipolyse bei übergewichtigen älteren Diabetikern, die die Fettzellrezeptoren, das Adenyl-Cyclase-System und die hormonempfindliche Lipase betreffen, wurden diskutiert.

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Anomalie de la lipolyse stimulée par l'adrénaline et la phentolamine dans le tissu adipeux provenant de diabétiques âgés et obèses

Résumé Les anomalies du métabolisme de la graisse dans des expériencesin vitro etin vivo ont été décrites ailleurs à la fois pour le diabète et l'obésité. Dans ces études, la libération de glycérol stimulée par l'adrénaline (100 M) et la phentolamine (100 g/ml) a été comparée dans le tissu adipeux provenant de groupes de sujets nondiabétiques, non-obèses, diabétiques et obèses. Le tissu adipeux des diabétiques obèses montrait une diminution très significative (p < 0.001) de la stimulation de la lipolyse par comparaison au tissu adipeux des non-diabétiques et des non-obèses. Les conditions de l'obésité et du diabète doivent être présentes simultanément pour maintenir cette différence dans la lipolyse. Le diabète ou l'obésité en eux-mêmes ne sont responsables que de différences à peine significatives dans la stimulation de la libération de glycérol. Nous avons discuté les raisons pouvant expliquer ce défaut de la lipolyse chez les diabétiques obèses et âgés concernant les récepteurs des cellules adipeuses, le système adényle-cyclase et la lipase dépendante de l'hormone.

     

Therapeutic actions of allylmercaptocaptopril and captopril in a rat model of metabolic syndrome

BACKGROUND: Hypertension often coexists with hyperlipidemia, insulin resistance, and glucose intolerance in metabolic syndrome. Allylmercaptocaptopril is a conjugate of the angiotensin-converting enzyme inhibitor captopril with allicin, an active principle in garlic with multiple beneficial actions on metabolic-syndrome abnormalities. We sought to test the hypothesis that the conjugation of allicin to captopril may confer additional therapeutic actions in metabolic disease. METHODS: We compared allylmercaptocaptopril (53.5 mg/kg/day orally for 60 days) to an equimolar dose of captopril (40 mg/kg/day) in the spontaneously hypertensive, obese rat (SHROB) model. RESULTS: Allylmercaptocaptopril prevented progressive weight gain, without a detectable effect on food intake. Both captopril and allylmercaptocaptopril lowered blood pressure, but allylmercaptocaptopril was more effective. Allylmercaptocaptopril, but not captopril, improved cardiac hypertrophy, as indicated by heart weight and ventricular-wall thickness. Allylmercaptocaptopril improved, whereas captopril impaired, oral glucose tolerance after a fast. Triglycerides were decreased by both captopril and allylmercaptocaptopril. Total cholesterol and non-HDL cholesterol were reduced by captopril but not by allylmercaptocaptopril. The SHROB rats developed severe glomerulosclerosis and renal failure. Allylmercaptocaptopril showed significant nephro-protection, as indicated by reductions in urinary protein loss, urinary protein-to-creatinine ratio, and plasma creatinine. Captopril showed the same trends and also prevented the decline of creatinine clearance. Finally, both allylmercaptocaptopril and captopril reduced the basal level of lipolysis in isolated abdominal adipocytes, and restored the response to catecholamine stimulation. CONCLUSIONS: Both captopril and allylmercaptocaptopril are effective in attenuating multiple abnormalities of metabolic syndrome. Allylmercaptocaptopril may have additional effectiveness on improving glucose tolerance, further lowering blood pressure, reducing cardiac hypertrophy, preventing weight gain, and protecting against renal disease.     

Pulsatile intravenous insulin replacement in streptozotocin-diabetic rats is more efficient than continuous delivery: effects on glycaemic control,insulin-mediated glucose metabolism and lipolysis

Summary Short-term exposure of tissues to pulses of insulin generally leads to an enhancement of insulin action. We have investigated the possible beneficial effects of long-term near-physiological continuous vs pulsatile intravenous insulin treatment of insulin-deficient streptozotocin (70 mg/kg) diabetic rats on blood glucose control, in vivo insulin action and in vitro insulin action in isolated adipocytes. First, we determined the 24-h peripheral plasma insulin profiles in normal rats under precisely controlled meal-feeding conditions. Basal plasma insulin levels (40±9 U/ml) oscillate with a periodicity of 11.9±0.9 min (p<0.05), and an amplitude of 60±10%. Subsequently, the 24-h insulin profile was mimicked in diabetic (D) rats by a continuous (c) or pulsatile (p) (6-min double, 6-min off) insulin infusion rate for 2 weeks, using a programmable pump-swivel unit. Control (C) rats received vehicle treatment. In Cc, Dc, Cp and Dp daily urinary glucose loss and average plasma glucose levels were 0±0, 7.5±4.4, 0±0, 0.8±0.4 mmol and 6.7±0.2, 11.5±2.7, 6.6±0.1, 5.9±1.4 mmol/l, respectively. Hypoglycaemia (<3 mmol/l) was observed in 10 and 20% of the blood samples collected from Dc and Dp rats, respectively. After 2 weeks of treatment, in vivo peripheral and hepatic insulin action was measured by the hyperinsulinaemic euglycaemic (6 mmol/l) clampwith[3-³H]-glucoseinfusion. Pre-clampcounter-regulatory hormone levels were similar among rats. Compared to Cc and Cp, Dc showed a reduction in insulin sensitivity and responsiveness for peripheral glucose uptake whereas Dp only showed a reduction in insulin sensitivity. Suppression of hepatic glucose production by insulin was similar among rats. After 2.5 weeks of treatment, epididymal adipocytes were isolated. Specific [¹²⁵I]-insulin binding, basal and insulin-stimulated [U-¹⁴C]-glucose uptake and isoproterenol-stimulated glycerol output were comparable among rat adipocytes. The inhibition of glycerol output by insulin was identical in Cp and Dp (V_max=48.6±6.1 and 42.3±4.6%) but blunted in Dc vs Cc (V_max=8.2±4.6 vs 44.0±7.2%, p<0.01) adipocytes, suggesting a post-binding defect in the antilipolytic action of insulin in Dc rats. In conclusion, long-term near-physiological pulsatile intravenous insulin replacement in insulin-deficient diabetic rats is more efficient than continuous delivery in reducing blood glucose, lowering glucosuria, increasing insulin sensitivity and inhibiting lipolysis.Abbreviations IDDM Insulin-dependent diabetes mellitus - AUC area under the curve - CV coefficient of variation     

Effects of Pineal Indoles and Arginine Vasotocin on Lipolysis and Lipogenesis in Isolated Adipocytes

The effects of arginine vasotocin and the pineal indoles melatonin, serotonin, N-acetylserotonin, hydroxytryptophol, methoxytryptophol, hydroxyindoleacetic acid, methoxyindoleacetic acid, and methoxytryptamine on lipolysis and lipogenesis in isolated adipocytes were studied. Basal lipolysis was inhibited by all the indoles tested at a dose of 1 mumole except hydroxytryptophol. Methoxytryptamine and serotonin inhibited hormone-induced lipolysis in a dose-dependent manner and exhibited the highest antilipolytic activity in isolated rat, rabbit, and hamster adipocytes. However, their antilipolytic activity could not be overcome by increasing the dose of the lipolytic hormone. Dibutyryl cyclic AMP-induced lipolysis was also inhibited. All the pineal indoles tested were capable of suppressing basal and insulin-stimulated lipogenesis in the dose range 0.33-3 nmole. At lower doses there was no effect. Arginine vasotocin at a dose of 25 nmole significantly augmented basal lipogenesis.     

The interaction of hCG with rat adipose tissue: apparent lack of hCG--LH receptors.

The interaction of human chorionic gonadotropin (hCG) with rat adipose tissue was investigated by both metabolic and binding studies. Highly purified preparations of hCG did not affect the adenylate cyclase activity nor the lipolysis of rat adipocytes in the presence or in the absence of GTP. However, it was demonstrated that (a) the hCGs used were biologically active since they stimulated cAMP and testosterone production by rat Leydig cells, and (b) there are receptor sites on the rat ovary that bind [125I]hCG and recognize rat luteinizing hormone (LH). The lack of response cannot then be attributed to a loss of activity of the hormone preparation tested nor to a failure of the rat tissues to recognize an hormone of human origin, but rather to an absence of hCG--LH receptors on the fat cell membrane surface. It is suggested that results previously reported in other laboratories could be explained by the presence of contaminating amounts of lipolytic hormones in their preparations.     

Localization and function of myocardial lipolysis

Summary Mobilization of triacylglycerol stored in heart cells is accomplished by the combined action of lysosomal (acid) lipase and microsomal monoacylglycerol lipase or carboxylesterase. Non(heparin)-releasable neutral or alkaline lipase is similar to non(readily)-releasable lipoprotein lipase (LPL). The enzyme is mainly localized extracellularly. Non(readily)-releasable LPL probably represents LPL in caveola or vacuolae of vascular endothelium and/or LPL on myocardial interstitium. It contributes to the uptake of lipoprotein constituents in heart cells. Glycerol, an endproduct of lipolysis, is not a reliable marker for the net mobilization of lipid stored in heart cells. It is formed both intra- and extracellularly, and does not reflect the rate of oxidation of part of free fatty acids formed.     

Comparative effects of thyroid hormone analogs on the activities of brain and liver mitochondria and nuclei in thyroidectomized rats

Several thyroid hormone analogs have been tested for thyromimetic activity on rat brain and liver subcellular organelles. The compounds were administered immediately after thyroidectomy to 90 g male S-D rats for 10 days, by daily s.c. injection. In cerebral cortex and liver we measured the activities of mitochondrial succinate cytochrome c reductase and a-GPD, and nuclear RNA polymerase I. Brain mitochondrial enzymes were unchanged in thyroidectomized (Tx) and in Tx-treated rats, whereas the activities of these enzymes in liver mitochondria were partially restored by the treatments. RNA polymerase I activity in brain and liver dropped significantly 10 days after thyroidectomy and daily injection of thyroid hormones or analogs maintained the nuclear activity at a normal level. Correlation between the structure of thyroid hormone analogs and their subcellular effects is in good agreement with previous binding and in vivo studies. Enzyme activities stimulated by T₃ were lowered by replacing the T₃ side-chain by an acetic acid group or by substituting the bridged oxygen atom by atom by CO. In contrast, the activity was enhanced by substituting iodine with a 3' isopropyl group. Although less active than iodine, the 3,5-dimethyl substituents may be introduced without a complete loss of nuclear activity.     

Role of the natriuretic peptide system in lipogenesis/lipolysis

AIM: There is recent evidence that the natriuretic peptide (NP) system promotes adipose tissue lipolysis in primates. This effect is mediated by the interaction of NP with its active receptors through guanylyl cyclase activation and cGMP production. This review will briefly focus on the new aspects of NP pathophysiology in man. DATA SYNTHESIS: NP receptors have been described in rodent adipocytes, and the expression of their mRNA is found in human adipose tissue together with high level of ANP binding sites. In isolated fat cells, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were able to stimulate lipolysis as much as isoproterenol, a non-selective beta-adrenergic receptor agonist, whereas C-type natriuretic peptide (CNP) had the lowest lipolytic effect. The potent lipolytic effect of NP has also been confirmed in samples of abdominal adipose tissue from healthy subjects. The potency order of the lipolytic effect (ANP > BNP > CNP) and ANP-induced cGMP production supported the presence of type A natriuretic peptide receptor in human fat cells. The effect of NP on lipid metabolism is confirmed by the fact that intravenous ANP infusion is followed by plasma NEFA and glycerol concentration increase (reflecting lipid mobilisation). CONCLUSIONS: The NP system seems to play an important role in lipid metabolism, possibly affecting the pathophysiology of obesity and obesity-related disorders, such hypertension. Further studies, however, are needed to completely establish the mechanisms involved in NP-induced lipolysis and the real relevance of this new pathway specific of primates.     

Interleukin-6 stimulates lipolysis in porcine adipocytes

Interleukin (IL)-6 stimulates lipolysis in human and rodents adipocytes. However, the mechanism regulating this process is little known. In this study, we demonstrated that IL-6 increased lipolysis in differentiated porcine adipocytes by activation of extracellular signal-related kinase (ERK), which was inhibited by specific ERK inhibitor PD98059. IL-6 treatment did not elevate intracellular cAMP and specific PKA inhibitor H89 did not affect IL-6-induced lipolysis, which suggested that protein kinase A (PKA) pathway was not involved in IL-6-induced lipolysis. Also, the expressions of perilipin A and PPARγ2 were significantly reduced in response to IL-6 treatment, but the expressions of peroxisome proliferators-activated receptor gamma coactivator-1 alpha (PGC-1α), carnitinepalmitoyl-transferase-1 (CPT-1), and uncoupling protein 2 (UCP2) were significantly elevated. In conclusion, these results suggested that chronic high dose of IL-6 directly stimulated lipolysis in porcine adipocytes through activation of ERK, subsequently repressing perilipin A and promoting PGC-1α expression.     

急性乙型肝炎患者血清甲状腺激素水平变化

目的研究急性乙型肝炎患者血清中甲状腺激素水平变化情况,观察患者甲状腺激素水平的动态变化和甲状腺激素水平异常与发病时间的关系。方法急性乙型肝炎患者36例作为观察对象,健康体检的36人作为对照组。检测其入院时的甲状腺激素水平：血清总甲状腺素（TT4）、血清总三碘甲腺原氨酸（TT3）、血清游离甲状腺素（FT4）、血清游离三碘甲腺原氨酸（FT3）、促甲状腺激素（TSH）,并与对照组比较。对异常者1周后复查甲状腺激素水平,以后每周复查1次,直至正常,观察其动态变化。结果急性乙型肝炎患者血清甲状腺激素TT4、TT3、FT4、FT3水平较对照组增高,差异具有统计学意义（P〈0.05）。TSH较对照组降低,但TSH均在正常值范围内,差异无统计学意义（P〉0.05）。入院时TT4、TT3、FT4、FT3高于正常值者在第三周全部转为正常。结论急性乙型肝炎患者血清甲状腺激素TT4、TT3、FT4、FT3水平升高,对于升高超过正常值者不需要治疗,随着肝功能逐渐好转,短期可恢复正常。