Obesity-prone rats have preexisting defects in their counterregulatory response to insulin-induced hypoglycemia.

Obesity-prone rats have preexisting defects in their counterregulatory response to insulin-induced hypoglycemia.
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易肥胖大鼠在对胰岛素引起的低血糖的反调节反应中存在预先存在的缺陷。

DOI:
10.1152/ajpregu.00312.2004
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发表时间:
2004
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
Levin,BarryE
Levin,BarryE
中科院分区:
--
文献类型:
--
作者:
Tkacs,NancyC;Levin,BarryE

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与饮食抵抗(DR)大鼠相比,在31%脂肪[高能量(HE)]饮食中发生饮食诱导肥胖(DIO)的大鼠对葡萄糖水平变化的感知和反应存在缺陷。因此,我们推测,他们也将有缺陷的反调节反应(CRR)胰岛素诱导的低血糖症(IIH)。饲料喂养的选择性繁殖的DIO和DR大鼠进行了三个连续的60分钟的间歇性间歇性出血,间隔48小时。葡萄糖水平迅速下降,但DIO大鼠的血浆肾上腺素(Epi)水平在前两次比赛中比DR大鼠低22-29%。在第三次试验中,尽管Epi水平相当,DIO大鼠在静脉注射葡萄糖后30分钟的葡萄糖水平较低,并且在静脉注射葡萄糖后85分钟反弹少于DR大鼠。虽然DIO大鼠获得更多的尸体和脂肪重量后4周的HE饮食比DR大鼠,他们不受先前IIH。与对照组相比,先前IIH和HE饮食的DR大鼠具有更高的弓状核神经肽Y(50%)和阿黑皮素原(POMC; 37%)mRNA,并且在HE饮食上POMC表达与体重增加之间呈负相关(r= 0.85;P= 0.004)。这些数据表明,DIO大鼠有一个预先存在的缺陷,在他们的CRR IIH,但IIH不影响他们的下丘脑神经肽的表达或体重增加,因为它在DR大鼠。
Rats that develop diet-induced obesity (DIO) on a 31% fat [high-energy (HE)] diet have defective sensing and responding to altered glucose levels compared with diet-resistant (DR) rats. Thus we postulated that they would also have defective counterregulatory responses (CRR) to insulin-induced hypoglycemia (IIH). Chow-fed selectively bred DIO and DR rats underwent three sequential 60-min bouts of IIH separated by 48 h. Glucose levels fell comparably, but DIO rats had 22–29% lower plasma epinephrine (Epi) levels during the first two bouts than DR rats. By the third trial, despite comparable Epi levels, DIO rats had lower 30-min glucose levels and rebounded less than DR rats 85 min after intravenous glucose. Although DIO rats gained more carcass and fat weight after 4 wk on an HE diet than DR rats, they were unaffected by prior IIH. Compared with controls, DR rats with prior IIH and HE diet had higher arcuate nucleus neuropeptide Y (50%) and proopiomelanocortin (POMC; 37%) mRNA and an inverse correlation (r= 0.85;P= 0.004) between POMC expression and body weight gain on the HE diet. These data suggest that DIO rats have a preexisting defect in their CRR to IIH but that IIH does not affect the expression of their hypothalamic neuropeptides or weight gain as it does in DR rats.