Cell cycle analysis in bone marrow and kidney tissues of dietary restricted rats

Diabesity: A Polygenic Model of Dietary-Induced Obesity from Ad Libitum Overfeeding of Sprague–Dawley Rats and Its Modulation by Moderate and Marked Dietary Restriction

“…Since the rate of estrone production is related to the fat mass, it may contribute significantly to the cancer risks for endometrial and mammary gland cancers and early development of reproductive dysfunction due to the abnormal amounts of estrogenic compounds produced in obese individuals (Bray, 2002;Small et al, 2002). In addition, DRfed rodents have an induction of the expression of SIRT1 deacetylase in numerous tissues, including visceral fat pads, and this causes the sequestration of the apoptotic factor BAX from mitochondria, preventing stress-induced apoptotic cell death and extending life (Lu et al, 1991;Cohen et al, 2004;Rhodes, 2005). Thus, obesity due to AL-overfeeding may be a causative factor in the large number of spontaneous metabolic, endocrine, reproductive, cardiovascular and neoplastic complications seen in diabesity, and DR-feeding induces healthful modulations.…”

“…Adult-onset human or animal type 2 diabetes associated with obesity (diabesity) is induced by a complex set of genetic, dietary and environmental interactions (Weindruch and Walford, 1988;Klinger et al, 1996;Brunner et al, 2001;Eckel et al, 2002;Bray, 2002). For example, monogenic obesity mutations in rodents such as those in the leptin gene (Lep ob , ob/ob mice) or its receptor gene (Lepr db , db/db mice, Lepr fa fa/fa Zucker rats or Lepr cp cplcpJCR rats) have been extremely useful in the study of these processes and useful in efficacy testing of anti-obesity and antidiabetic drugs (Harrison and Archer, 1987;Lee and Yu, 1990;Lu et al, 1991;Leiter, 2002;Inui et al, 2004;Park and Prolla, 2005). However, the monogenic basis of these mutated inbred rodent models does not reflect the more common forms of human obesity and adult-onset type 2 diabetes (diabesity) which are known to be a polygenic syndrome in heterozygous human populations (Klinger et al, 1996;Whitaker et al, 1997;Eckel et al, 2002;Hursting et al, 2003;Konstantinov, 2003;Rauser et al, 2003;Park and Prolla, 2005).…”

Hepatic nuclear ploidy distribution of dietary-restricted mice.

“…To measure hepatic nuclear ploidy classes in mice, a modified method of Vindelov et al (33) was used for staining nuclei. A nuclear suspension of the liver tissue was prepared from frozen tissue as described previously (26). Briefly, liver was minced with fine scissors in buffer solution, and nuclei were isolated by trypsinization of the tissue suspension.…”

“…However, its mode of action remains to be elucidated. DR may inhibit cell division in specific tissues in rats (25)(26) and mice (27) and, perhaps, inhibits the growth of normal cells and/or cell variants that have the capacity to become neoplastic.…”

Estudo morfoquantitativo e imunohistoquímico da cartilagem articular do joelho de ratos Wistar submetidos à restrição calórica no envelhecimento

“…A restrição alimentar, caracterizada pela redução da quantidade de alimento diário, respeitando o conceito de "subnutrição sem desnutrição", causa mudanças significativas na porcentagem de células em todas as fases do ciclo celular na medula óssea (LU et al, 1991), inibe a proliferação celular no baço e timo de ratos jovens (LU et al, 1993), além disso, aumenta a longevidade de diversas espécies, incluindo ratos. Hipóteses sugerem que esse efeito de prolongamento da vida é mediado por uma mudança no estado biológico de proliferação celular e reprodução para um, no qual, a manutenção celular e mecanismos de reparo são maximizadas (HOLLOSZY, 1997 Estudos mostram que mudanças na ingestão calórica, podem alterar diversas variáveis fisiológicas e comportamentais (HART et al, 1999) como temperatura basal do organismo e a atividade metabólica (DUFFY et al, 1990); induzir uma mudança bem coordenada entre carboidrato e metabolismo gordo (mensurado pela análise do cociente respiratório), resultando de alterações de níveis hormonais e/ou modulação da atividade do receptor hormonal (ALY et al, 1994); diminuir a atividade reprodutora trocada pelo objetivo de busca alimentar; modificar a habilidade do organismo em prevenir infecções; causar alterações na regulação do dano, reparo, replicação e expressão do DNA para manutenção da integridade do genoma (HART; TURTURRO, 1997;HART et al, 1999).…”