Mari Renata de Britto, Stabille Sandra Regina, de Faria Haroldo Garcia, Pereira Joice Naiara Bertaglia, Guimarães Juliana Plácido, Marinsek Gabriela Pustiglione, de Souza Romeu Rodrigues
a São Paulo State University (Unesp) , Institute of Biosciences , São Vicente , São Paulo , Brazil.
b Department of Morphological Sciences , Maringá State University , Maringá , Paraná , Brazil.
J Diet Suppl. 2018 May 4;15(3):285-299. doi: 10.1080/19390211.2017.1341446. Epub 2017 Jul 31.
Aging can promote significant morphofunctional changes in the gastrointestinal tract (GIT). Regulation of GIT motility is mainly controlled by the myenteric neurons of the enteric nervous system. Actions that aim at decreasing the aging effects in the GIT include those related to diet, with caloric restriction (CR). The CR is achieved by controlling the amount of food or by manipulating the components of the diet. Therefore, the objective of this study was to evaluate different levels of CR on the plasticity of nicotinamide adenine dinucleotide phosphate- (NADPH-) reactive myenteric neurons in the colon of Wistar rats during the aging process using ultrastructural (transmission electron microscopy) and morphoquantitative analysis. Wistar male rats (Rattus norvegicus) were distributed into 4 groups (n = 10/group): C, 6-month-old animals; SR, 18-month-old animals fed a normal diet; CRI, 18-month-old animals fed a 12% CR diet; CRII, 18-month-old animals fed a 31% CR diet. At 6 months of age, animals were transferred to the laboratory animal facility, where they remained until 18 months of age. Animals of the CRI and CRII groups were submitted to CR for 6 months. In the ultrastructural analysis, a disorganization of the periganglionar matrix with the aging was observed, and this characteristic was not observed in the animals that received hypocaloric diet. It was observed that the restriction of 12.5% and 31% of calories in the diet minimized the increase in density and cell profile of the reactive NADPH neurons, increased with age. This type of diet may be adapted against gastrointestinal disturbances that commonly affect aging individuals.
衰老会促使胃肠道（GIT）发生显著的形态功能变化。胃肠道运动的调节主要由肠神经系统的肌间神经元控制。旨在减少胃肠道衰老影响的措施包括与饮食相关的措施，如热量限制（CR）。热量限制可通过控制食物量或调整饮食成分来实现。因此，本研究的目的是利用超微结构（透射电子显微镜）和形态定量分析，评估不同水平的热量限制对衰老过程中Wistar大鼠结肠中烟酰胺腺嘌呤二核苷酸磷酸（NADPH）反应性肌间神经元可塑性的影响。Wistar雄性大鼠（褐家鼠）被分为4组（每组n = 10）：C组，6月龄动物；SR组，18月龄正常饮食动物；CRI组，18月龄摄入12%热量限制饮食的动物；CRII组，18月龄摄入31%热量限制饮食的动物。6月龄时，将动物转移至实验动物设施，直至18月龄。CRI组和CRII组的动物进行6个月的热量限制。在超微结构分析中，观察到随着衰老神经节周围基质出现紊乱，而在摄入低热量饮食的动物中未观察到这一特征。观察到饮食中12.5%和31%的热量限制可使随着年龄增长而增加的反应性NADPH神经元的密度和细胞轮廓的增加最小化。这种饮食方式可能适用于对抗通常影响老年人的胃肠道紊乱。
