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Tamanho da fonte: 
OBESITY ONSET DUE TO LOW-PROTEIN DIET IN ADOLESCECE IS NOT ASSOCIATED WITH HYPOTHALAMIC LEPTIN RESISTANCE
Bárbara Letícia Antonio Membrive, Hercules de Oliveira Costermani, Sara Santos dos Reis, Amanda Freitas da Silva, Dayane Oliveira Melo, Ginislene Dias Souza Miranda

Última alteração: 09-10-18

Resumo


Calorie restriction in experimental models, at adolescence, malprograms to metabolic impairments, like that it happens in intrauterine rat models.

We aimed to assess the leptin signaling pathway in the hypothalamus in both adolescent and adult rats that were malnourished at puberty.

At 30-days-old, Wistar male rats were fed a low-protein diet (4%, LP group) until 60-days-old and then, to dietary rehabilitation, were fed a normal-protein diet (20.5%) from 60- to 120-days-old. Control rats (NP group) were fed a normal-protein diet throughout life. Body weight and food intake were evaluated throughout experimental period. At 60- and 120-days-old, a batch of rats was euthanized to remove visceral fat pad (mesenteric fat), blood and hypothalamus to quantify body fat deposition by biometrical analysis, leptinemia by ELISA and leptin signaling by western blot. Experimental procedures were approved by the research ethical committee for use of animals from the Universidade Federal de Mato Grosso (protocol: 23108.709618/2015-21). All data were analyzed by Student t test, through Graph Pad Prism, for Windows.

At 60-days-old, after starvation period, LP-rats showed smaller body weight (–72%, P<0.001) and mesenteric fat-pad stores (–39%, P<0.01), hypophagia (–30%, P<0.001) and hypoleptinemia (–82%, P<0.001) than NP-rats. By contrast, at 120-days-old LP-rats displayed higher body weight gain (+94%, P<0.001) and mesenteric fat-pad stores (+28%, P<0.01) than NP-rats. In addition, LP-rats were hyperphagic (+26%, P<0.001) and hyperleptinemic (+105%, P<0.001). Interestingly, although SOCS3 were reduced in LP-rats at both 60- (–26%, P<0.05) and 120-days-old (–49%, P<0.05) all of other proteins from the leptin signaling-pathway did not change in both ages (P>0.05).

Obesity development in adult rats, malnourished at puberty, is not due to central leptin resistance, but possibly by other neuroendocrine factors that can be affecting energy balance.


Palavras-chave


Metabolic programming, obesity, metabolic syndrome, hypothalamus, leptin signaling.