Plasma leptin in diabetic and insulin-treated diabetic and normal rats.

Plasma leptin in diabetic and insulin-treated diabetic and normal rats.
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糖尿病和胰岛素治疗的糖尿病大鼠和正常大鼠的血浆瘦素。

DOI:
10.1016/s0026-0495(98)90244-x
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发表时间:
1998
期刊:
Metabolism: clinical and experimental
影响因子:
--
通讯作者:
Leibel,RL
Leibel,RL
中科院分区:
--
文献类型:
--
作者:
Sivitz,WI;Walsh,S;Morgan,D;Donohoue,P;Haynes,W;Leibel,RL

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脂肪组织瘦素mRNA水平下降的食物剥夺或诱导胰岛素缺乏型糖尿病。为了确定血浆瘦素浓度是否受到类似的影响,是否用胰岛素治疗糖尿病恢复血浆瘦素,以及这是否需要恢复体重(由于糖尿病而丢失)和/或体重正常化,我们测量了对照组、未治疗的链脲佐菌素(STZ)糖尿病大鼠和胰岛素治疗的STZ糖尿病大鼠的血浆瘦素浓度。未治疗的STZ糖尿病大鼠血浆瘦素显着减少。胰岛素治疗4至17天增加血浆瘦素约两倍以上的控制水平。然而,尽管高瘦素血症,胰岛素治疗的糖尿病大鼠体重增加的速度等于假治疗的对照组。在17天胰岛素治疗的糖尿病大鼠附睾脂肪组织瘦素mRNA水平是相等的,但没有超过假对照水平,不像血浆瘦素。胰岛素治疗的STZ糖尿病大鼠的血糖浓度低于假手术对照组。因此,为了确定低血糖是否在增加血浆瘦素中可能是重要的,我们测量了用胰岛素输注3小时的糖尿病大鼠的血浆瘦素水平,所述胰岛素输注沿着以200或40 mg/100 mL为目标的可变速率葡萄糖输注。血浆瘦素迅速增加,在这些大鼠无论目标体重。正常大鼠输注胰岛素和葡萄糖(目标剂量,200 mg/100 mL)后,血浆瘦素也迅速升高。我们的结论是,血浆瘦素浓度显着降低胰岛素缺乏的条件下,迅速增加胰岛素治疗。血浆瘦素的增加不需要体重的恢复,并且在葡萄糖钳夹条件下,不依赖于靶向瘦素。胰岛素治疗的糖尿病大鼠的高瘦素血症不能根据稳态瘦素mRNA水平来解释,至少在附睾脂肪中反映了这一点。
Adipose tissue leptin mRNA levels are decreased by food deprivation or induction of insulin-deficient diabetes. To determine whether plasma leptin concentrations are similarly affected, whether treatment of diabetes with insulin restores plasma leptin, and whether this requires restoration of body weight (lost as a result of diabetes) and/or normalization of glycemia, we measured plasma leptin concentrations in control, untreated streptozotocin (STZ)-diabetic, and insulin-treated STZ-diabetic rats. Plasma leptin was markedly reduced in untreated STZ-diabetic rats. Insulin treatment for 4 to 17 days increased plasma leptin approximately twofold above control levels. However, despite the hyperleptinemia, insulin-treated diabetic rats gained weight at a rate equal to that of sham-treated controls. Epididymal adipose tissue leptin mRNA levels in 17-day insulin-treated diabetic rats were equal to but did not exceed sham-control levels, unlike plasma leptin. Plasma glucose concentrations in insulin-treated STZ-diabetic rats were lower than in sham controls. Therefore, to determine whether hypoglycemia may be important in increasing plasma leptin, we measured plasma leptin levels in diabetic rats infused with insulin for 3 hours along with a variable-rate glucose infusion targeting glycemia to 200 or 40 mg/100 mL. Plasma leptin rapidly increased in these rats irrespective of target glycemia. Plasma leptin also increased rapidly in normal rats infused with insulin and glucose (target glycemia, 200 mg/100 mL). We conclude that plasma leptin concentrations are markedly reduced under conditions of insulin deficiency and rapidly increased by insulin treatment. The increase in plasma leptin does not require restoration of body weight and, under glucose clamp conditions, does not depend on target glycemia. Hyperleptinemia in insulin-treated diabetic rats is not explained on the basis of steady-state leptin mRNA levels, at least as reflected in epididymal fat.
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DOI: 10.1210/endo.138.8.5327
发表时间: 1997
期刊: Endocrinology.
影响因子: --
作者:
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DOI: --
发表时间: 1997
影响因子: 5.8
作者:
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DOI: 10.1210/mend-4-4-583
发表时间: 1990
期刊: Molecular endocrinology (Baltimore, Md.)
影响因子: --
作者:
Sivitz,WI;DeSautel,SL;Kayano,T;Bell,GI;Pessin,JE
通讯作者: Pessin,JE
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DOI: 10.1016/s0014-5793(96)01477-9
发表时间: 1997
期刊: FEBS Letters
影响因子: 3.5
作者:
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