Metabolic defense of the body weight set-point.

Metabolic defense of the body weight set-point.
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体重设定点的代谢防御。

DOI:
10.3928/0048-5713-19831101-03
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发表时间:
1983
期刊:
Research publications - Association for Research in Nervous and Mental Disease
影响因子:
--
通讯作者:
S. Corbett
S. Corbett
中科院分区:
--
文献类型:
--
作者:
R. E. Keesey;S. Corbett

文献摘要

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生物体的能量需求是其维持的组织质量的函数。种间比较表明,能量需求是体重的幂函数 (12)。这里描述的大部分工作都试图确定将种内能量消耗与维持体重相关的函数是否采取类似的形式。迄今为止,来自各种大鼠制剂的证据表明,尽管可能存在一些差异,但大鼠的功能形式不太可能与 Kleiber 得出的种间功能有很大差异 (12)。然而,这项工作还表明,只有当生物体处于其通常维持和防御的特定体重时,种间和种内功能才能准确预测能量需求。这是因为体重从正常水平增加会导致能量需求以比关系预测的更快的速度增加,而体重从正常水平下降会产生比预测的能量消耗减少更大的速度。因此,我们建议将动物的体重设定点视为可以根据其代谢体型准确预测其每日能量需求的体重。只有在这一体重下,动物的代谢才正常。然后可以询问维持异常高或低体重的生物体是否患有调节功能障碍或调节正常但处于升高或降低的设定点。我们已经看到,肥胖的 Zucker 大鼠与正常体重的大鼠一样,表现出与体重减轻相同的适应性代谢调整。由于种内体重与代谢需求关系的确切形式尚未确定,因此我们必须保留对 Zucker 脂肪大鼠在体重升高时是否代谢正常的判断。然而,由于它们对肥胖表现出有效的代谢防御,因此设定点升高,而不是监管失败,似乎是扎克脂肪状况更可能的原因。 LH 损伤的大鼠提供了更令人信服的体重设定值调节调节证据。该制剂在其维持的体重降低时处于正常代谢状态,而当其体重升高至未病变同窝小鼠的水平时,其变为代谢亢进状态。另一方面,VMH 损伤大鼠的肥胖很可能源于主要的调节损伤。(摘要截断为 400 字)
The energy needs of an organism are a function of the tissue mass it maintains. Interspecific comparisons indicate that energy needs are a power function of body weight (12). Much of the work described here represents an effort to ascertain whether the function relating intraspecific energy expenditure to maintained body weight takes a similar form. The evidence to date from various rat preparations suggests that although some differences may exist, the form of the function for rats is not likely to differ substantially from the interspecific function derived by Kleiber (12). What has also emerged from this work, however is evidence that both the inter- and intraspecific functions accurately predict energy needs only when the organism is at the particular body weight it normally maintains and defends. This is because a rise in weight from the normal level causes energy needs to increase at a faster rate than the relationship would predict, whereas declines in weight from this level produce greater than predicted decreases in energy expenditure. We thus propose that an animal's body weight set-point be taken as the weight at which its daily energy needs can be accurately predicted from its metabolic body size. It is only at this one body weight that the animal is normometabolic. It can then be asked whether organisms maintaining abnormally high or low body weights are suffering from regulatory dysfunctions or regulating normally but at elevated or depressed set-points. We have seen that obese Zucker rats display the same adaptive metabolic adjustments to weight loss as normal weight rats. Since the exact form of the intraspecific body weight-metabolic needs relationship has not yet been determined, we must withhold judgment as to whether Zucker fatty rats are normometabolic at their elevated body weights. Since they display an effective metabolic defense of their obesity, however, an elevated set-point, rather than regulatory failure, seems to be the more probable cause of the Zucker fatty's condition. More compelling evidence of regulation at an altered body weight set-point is provided by the LH-lesioned rat. This preparation is normometabolic at the reduced body weight it maintains, and it becomes hypermetabolic when its weight is elevated to the level of nonlesioned littermates. The obesity of the VMH-lesioned rat, on the other hand, may well stem from primary regulatory impairments.(ABSTRACT TRUNCATED AT 400 WORDS)