Search Results

You are looking at 1 - 2 of 2 items for

  • Author: Flávio Andrade Francisco x
  • All content x
Clear All Modify Search
Restricted access

Tatiane Aparecida Ribeiro, Audrei Pavanello, Laize Peron Tófolo, Júlio Cezar de Oliveira, Ana Maria Praxedes de Moraes, Claudinéia Conationi da Silva Franco, Kelly Valério Prates, Isabela Peixoto Martins, Kesia Palma-Rigo, Rosana Torrezan, Erica Yeo, Rodrigo Mello Gomes, Flávio Andrade Francisco, Paulo Cezar de Freitas Mathias, and Ananda Malta

We tested whether chronic supplementation with soy isoflavones could modulate insulin secretion levels and subsequent recovery of pancreatic islet function as well as prevent metabolic dysfunction induced by early overfeeding in adult male rats. Wistar rats raised in small litters (SL, 3 pups/dam) and normal litters (NL, 9 pups/dam) were used as models of early overfeeding and normal feeding, respectively. At 30 to 90 days old, animals in the SL and NL groups received either soy isoflavones extract (ISO) or water (W) gavage serving as controls. At 90 days old, body weight, visceral fat deposits, glycemia, insulinemia were evaluated. Glucose-insulin homeostasis and pancreatic-islet insulinotropic response were also determined.

The early life overnutrition induced by small litter displayed metabolic dysfunction, glucose and insulin homeostasis disruption in adult rats. However, adult SL rats treated with soy isoflavones showed improvement in glucose tolerance, insulin sensitivity, insulinemia, fat tissue accretion and body weight gain, compared with SL-W group. Pancreatic-islet response to cholinergic, adrenergic and glucose stimuli was improved in both isoflavone-treated groups. In addition, different isoflavone concentrations increased glucose-stimulated insulin secretion in islets of all groups with higher magnitude in both NL and SL isoflavone treated groups. These results indicate that long-term treatment with soy isoflavones inhibits early overfeeding-induced metabolic dysfunction in adult rats and modulated the process of insulin secretion in pancreatic islets.

Free access

Isis Gabrielli Barbieri de Oliveira, Marcos Divino Ferreira Junior, Paulo Ricardo Lopes, Dhiogenes Balsanufo Taveira Campos, Marcos Luiz Ferreira-Neto, Eduardo Henrique Rosa Santos, Paulo Cezar de Freitas Mathias, Flávio Andrade Francisco, Bruna Del Vechio Koike, Carlos Henrique de Castro, André Henrique Freiria-Oliveira, Gustavo Rodrigues Pedrino, Rodrigo Mello Gomes, and Daniel Alves Rosa

Disruptions in circadian rhythms have been associated with several diseases, including cardiovascular and metabolic disorders. Forced internal desynchronization induced by a period of T-cycles of 22 h (T22 protocol) reaches the lower limit of entrainment and dissociates the circadian rhythmicity of the locomotor activity into two components, driven by different outputs from the suprachiasmatic nucleus (SCN). The main goal of this study was to evaluate the cardiovascular and metabolic response in rats submitted to internal desynchronization by T22 protocol. Male Wistar rats were assigned to either a control group subjected to a usual T-cycles of 24 h (12 h–12 h) or an experimental group subjected to the T22 protocol involving a 22-h symmetric light–dark cycle (11 h–11 h). After 8 weeks, rats subjected to the T22 exhibited desynchrony in their locomotor activity. Although plasma glucose and insulin levels were similar in both groups, desynchronized rats demonstrated dyslipidemia, significant hypertrophy of the fasciculate zone of the adrenal gland, low IRB, IRS2, PI3K, AKT, SOD and CAT protein expression and an increased expression of phosphoenolpyruvate carboxykinase in the liver. Furthermore, though they maintained normal baseline heart rates and mean arterial pressure levels, they also presented reduced baroreflex sensitivity. The findings indicate that circadian timing desynchrony following the T22 protocol can induce cardiometabolic disruptions. Early hepatic metabolism dysfunction can trigger other disorders, though additional studies are needed to clarify the causes.