Aspergillosis is a disease that predominantly affects immunocompromised patients. The incidence in immunocompetents is rare, and manifestation is generally pulmonary. Few reports in the literature refer to isolated cerebral aspergillosis in individuals with no chronic comorbidities. We describe a case of a 59-year-old rural worker without previous pathologies who had a partial convulsive crisis in a subtle form, with self-limiting and nonrecurrent secondary generalization. Diagnostic investigation demonstrated a subcortical tumorlike lesion in the right precentral gyrus by nuclear magnetic resonance that allowed en bloc microsurgical resection, with histopathologic findings indicating cerebral aspergillosis. Because of the delay in obtaining the result of the biopsy due to technical difficulties with analysis, the diagnosis was delayed. The patient was clinically stable, with imaging without modifications and with negative serologic tests, so it was decided to follow the patient without antifungal therapy, which was successful. This was a case of isolated cerebral aspergillosis in an immunocompetent individual who was successfully treated by complete resection of the lesion alone, without combined antifungal therapy.

Early life overfeeding in the rat can be experimentally induced by reducing litter size. This investigation assessed the consequences of this manipulation on glucose metabolism in vivo and in isolated hepatocytes in 150-day old rats. Additionally, after body growth, the effects of caloric restriction and refeeding were tested. Adult rats from control (G9) and reduced litters (G3L) did not differ in body and fat weights, glucose tolerance or insulin resistance (insulin-induced hypoglycemia), or hepatocyte glucose release under basal or gluconeogenic conditions. Caloric restriction (G3R) reduced body and fat weights, decreased glucose decay after insulin injection and decreased hepatocyte gluconeogenic glucose release. Refeeding after caloric restriction reversed these parameters to those of the freely-fed groups (G9 and G3L). Taken together, these results suggest that the liver glucose metabolism is not programmed by lactational overfeeding, but rather is responsive to the current nutritional condition of the animal.

BACKGROUNDS: The Western diet (high in fat and sucrose) consumption is a highly prevalent feature in the whole world, mainly due to the increasing consumption of ultra-processed foods (UPF), which are cheaper and easier-to-eat, as compared to fresh and highly nutritive meals. Epidemiological studies have associated UPF consumption withdevelopment of obesity, non-alcoholic fat liver disease (NAFLD) and insulin resistance. For molecular studies, mice fed with Western diets have been used to characterize signaling pathways involved in these diet-induced pathologies, aiming to identify putative targets for treatments. However, these studies fed mice continuously with the diets, which is not compatible with what occurs in real life, when consumption is occasional. METHODS: Here, we fed mice once-a-week with a high fat, high sucrose (HFHS) diet and compared these animals with those fed continuously with HFHS diet or with a standard diet. RESULTS: Our results show that after a single day of consuming HFHS, animals presented impaired oral glucose tolerance test (oGTT) as compared to control group. Although this impairment was reversed after 24 hours consuming regular diet, repetition of HFHS consumption once-a-week aggravated the picture such as after 12-weeks, oGTT impairment was not reversed after 6 days under control diet. Liver steatosis, inflammation, impaired insulin signaling pathway and endoplasmic reticulum stress are similar comparing animals that consumed HFHS once-a-week with those that continuously consumed HFHS, though weekly-fed animals did not gain as much weight. CONCLUSIONS: Regimen of one day HFHS plus 6 days normal diet over 12 weeks is sufficient to induce insulin resistance and NAFLD in mice.

GB (goji berry) has bioactive components capable of reversing the metabolic syndrome. This work investigated systemic, biometric and metabolic parameters of male rats fed with standard diet (group CD) or high-carbohydrate diet (group HC). At 90 days of age the HC group was subdivided: one was given vehicle solution (HCD) and the other was given GB extract (HCDGB), for 60 days. The vehicle was also given to the CD group. At 150 days of age, glucose tolerance test, tissue collection, plasmatic determinations, lipid content, in situ perfusion and oxidative stress of the liver were carried out. The GB supplementation improved the parameters of the metabolic syndrome caused by the HC diet, including decreased body weight gain, adiposity index, dyslipidemia, hyperinsulinemia, NAFLD, liver oxidative stress and gluconeogenesis. Together with the diminished insulin resistance, these results indicate the GB extract is an important adjuvant in the treatment of the metabolic syndrome.

The Western diet (high in fat and sucrose) consumption is a highly prevalent feature in the whole world, mainly due to the increasing consumption of ultra-processed foods (UPF), which are cheaper and easier-to-eat, as compared to fresh and highly nutritive meals. Epidemiological studies have associated UPF consumption with development of obesity, non-alcoholic fat liver disease (NAFLD) and insulin resistance. For molecular studies, mice fed with Western diets have been used to characterize signaling pathways involved in these diet-induced pathologies. However, these studies fed mice continuously with the diets, which is not compatible with what occurs in real life, when consumption is occasional. Here, we fed mice once-a-week with a high fat, high sucrose (HFHS) diet and compared these animals with those fed continuously with HFHS diet or with a standard diet. Our results show that after a single day of consuming HFHS, animals presented impaired oral glucose tolerance test (oGTT) as compared to control group. Although this impairment was reversed after 24 h consuming regular diet, repetition of HFHS consumption once-a-week aggravated the picture such as after 12-weeks, oGTT impairment was not reversed after 6 days under control diet. Liver steatosis, inflammation, impaired insulin signaling pathway and endoplasmic reticulum stress are similar comparing animals that consumed HFHS once-a-week with those that continuously consumed HFHS, though weekly-fed animals did not gain as much weight. Therefore, we conclude that regimen of one day HFHS plus 6 days normal diet over 12 weeks is sufficient to induce insulin resistance and NAFLD in mice.