The consequences of seasonal fasting during the dormancy of tegu lizards (Salvator merianae) on their postprandial metabolic response.

Tegu lizards (Salvator merianae) aestivate for up to 5 months during Brazil's winter, when they retreat to burrows and halt most activities. Dormant tegus reduce their gastrointestinal (GI) mass, which allows a substantial energy economy. This strategy, however, implies that the first post-dormancy digestion would be more costly than subsequent feeding episodes as a result of GI atrophy. To address this, we determined the postprandial metabolic response (SDA) of the first (M1), second (M2) and several (RM) feeding episodes after tegus' dormancy. Another group of tegus (PF) was subjected to an extra 50 day fasting period after arousal. Glucose, triglycerides and uric acid levels were checked before and after feeding. M1 digestion lasted twice as long and cost twofold more when compared with M2 or RM, in agreement with the idea that GI atrophy inflates digestion cost at the first post-dormancy meal. The SDA response was similar in M2 and RM, suggesting that the GI tract was fully reorganized after the first feeding. The SDA cost was equal in PF and RM, implying that the change in state per se (dormant to arousal) triggers the regrowth of GI, independently of feeding. Fasting tegus at M1 presented higher triglyceride and lower uric acid levels than fed tegus, indicating that fasting is mainly sustained by fat storage. Our results show that seasonal fasting imposes an extra digestion cost to tegus following their next feeding, which is fully paid during their first digestion. This surplus cost, however, is negligible compared with the overall energetic savings from GI tract atrophy during the dormancy period.

Visceral fat increase and signals of inflammation in adipose tissue after administration of titanium dioxide nanoparticles in mice.

Titanium dioxide nanoparticles (TiO2 NP) are present in several daily use products, and the risks associated with their bioaccumulation must be stablished. Thus, an evaluation of several toxicological-related effects was conducted after intraperitoneal injection of TiO2 NPs in mice. Mice were divided into two groups, which received 2 mg kg-1 day-1 of TiO2 NPs or vehicle saline. Assessments of body and organ weight as well as biochemical, hematological, and histopathological analyses were performed in order to evaluate adverse effects. The results showed that treatment resulted in an increased visceral and abdominal fat deposition, as well as a mononuclear inflammatory infiltrates in the abdominal fat tissue. The TiO2 NPs induced significant decrease in the weight gain and splenomegaly. Additionally, TiO2 NP-treated mice showed altered hematological parameters and significant liver injuries, which were characterized by histopathological and biochemical changes. Our results also indicated that TiO2 NPs were absorbed and significantly accumulated in the spleen, liver, and kidney. These results showed the ability of TiO2 NPs to infiltrate different organs and to induce inflammation and liver and spleen damage with visceral fat accumulation. The data obtained are useful for the governmental authorities to legislate and implement regulations concerning the use and the production of this kind of material that might be hazardous to the living beings, as well as to the environment.