BackgroundTemporal restriction of food availability entrains circadian behavioral and physiological rhythms in mammals by resetting peripheral oscillators. This entrainment underlies the activity of a timing system, different from the suprachiasmatic nuclei (SCN), known as the food entrainable oscillator (FEO). So far, the precise anatomical location of the FEO is unknown. The expression of this oscillator is associated with an enhanced arousal prior to the food presentation that is called food anticipatory activity (FAA). We have focused on the study of the role played by the liver as a probable component of the FEO. The aim of this work was to identify metabolic and structural adaptations in the liver during the expression of the FEO, as revealed by histochemical assessment of hepatic glycogen and triacylglycerol contents, morphometry, and ultrastructure in rats under restricted feeding schedules (RFS).ResultsRFS promoted a decrease in the liver/body weight ratio prior to food access, a reduction of hepatic water content, an increase in cross-sectional area of the hepatocytes, a moderate reduction in glycogen content, and a striking decrease in triacylglyceride levels. Although these adaptation effects were also observed when the animal displayed FAA, they were reversed upon feeding. Mitochondria observed by electron microscopy showed a notorious opacity in the hepatocytes from rats during FAA (11:00 h). Twenty four hour fasting rats did not show any of the modifications observed in the animals expressing the FEO.ConclusionsOur results demonstrate that FEO expression is associated with modified liver handling of glycogen and triacylglycerides accompanied by morphometric and ultrastructural adaptations in the hepatocytes. Because the cellular changes detected in the liver cannot be attributed to a simple alternation between feeding and fasting conditions, they also strengthen the notion that RFS promotes a rheostatic adjustment in liver physiology during FEO expression.

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The coronavirus disease 2019 (COVID-19) pandemic was devastating worldwide. The introduction of severe acute respiratory syndrome coronavirus 2 vaccination has reduced transmission, hospitalizations, and deaths, with infrequent major side effects. We present the case of a 51-year-old woman with rapidly progressive glomerulonephritis following COVID-19 vaccination with ChAdOx1 (AstraZeneca). Workup and histopathologic examination demonstrated active extracapillary proliferative lesions in cellular and fibrocellular crescents with extensive fibrinoid necrosis and karyorrhexis with diffuse glomerulonephritis, as well as positive perinuclear antineutrophil cytoplasmic antibodies. Treatment with cyclophosphamide and steroids was initiated with the improvement of renal function. Similar cases were seen with influenza vaccination, potentially describing vaccination as a possible trigger for anti-myeloperoxidase rapidly progressive glomerulonephritis.

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