ABSTRACT
BACKGROUND: The activation of the hypothalamic-pituitary-adrenal (HPA) axis is essential for metabolic adaptation in response to fasting. However, the neurocircuitry connecting changes in the peripheral energy stores to the activity of hypothalamic paraventricular corticotrophin-releasing factor (CRFPVN) neurons, the master controller of the HPA axis activity, is not completely understood. Our main goal was to determine if hypothalamic arcuate nucleus (ARC) POMC and AgRP neurons can communicate fasting-induced changes in peripheral energy stores, associated to a fall in plasma leptin levels, to CRFPVN neurons to modulate the HPA axis activity in mice. RESULTS: We observed increased plasma corticosterone levels associate with increased CRFPVN mRNA expression and increased CRFPVN neuronal activity in 36 h fasted mice. These responses were associated with a fall in plasma leptin levels and changes in the mRNA expression of Agrp and Pomc in the ARC. Fasting-induced decrease in plasma leptin partially modulated these responses through a change in the activity of ARC neurons. The chemogenetic activation of POMCARC by DREADDs did not affect fasting-induced activation of the HPA axis. DREADDs inhibition of AgRPARC neurons reduced the content of CRFPVN and increased its accumulation in the median eminence but had no effect on corticosterone secretion induced by fasting. CONCLUSION: Our data indicate that AgRPARC neurons are part of the neurocircuitry involved in the coupling of PVNCRF activity to changes in peripheral energy stores induced by prolonged fasting.
ABSTRACT
OBJECTIVE: To evaluate the association of phase angle (PA) with clinical and nutritional aspects in patients with Parkinson's disease (PD) treated in an outpatient clinic in northeastern Brazil. METHODS: This is a case series study involving adults and the elderly with PD of both genders. We collected data such as stage, severity, and time of diagnosis of the disease, muscle strength, gait speed, and level of physical activity. We evaluated the nutritional status using body mass index, calf circumference, skeletal appendicular muscle mass index, and the presence of sarcopenia. We obtained the PA through the analysis by electrical bioimpedance. After obtaining the result of the division between reactance and resistance, with later transformation into degrees, we multiplied the result by 180/π. RESULTS: We evaluated 77 individuals with a mean age of 65.4 ± 8.9 years. 63.6% of them had reduced PA values and 19.7% of them had sarcopenia. Age (rho = - 0.423; p = < 0.001) was inversely correlated with PA. Skeletal appendicular muscle mass index (rho = 0.251; p = 0.028), pressure force (rho = 0.240; p = 0.035), and gait speed (rho = 0.323; p = 0.005) showed a direct correlation with age. When adjusted for confounding factors, only age remained associated with PA (p = 0.012). CONCLUSION: Most individuals had reduced PA, and only age was associated with this result. Aging is a risk factor for reducing muscle mass and physical disability in PD. Although this study indicates a relationship between PA, age, muscle mass, and functionality, further prospective studies are needed to confirm these findings.
