Changes in physical activity and alimentation habits during the initial phase of the covid-19 pandemic: a descriptive transversal study

Background: Physical exercise and healthy alimentation are considered the two basic columns for a healthy life. This study, objected to describe the impact of physical distancing in the initial phase of the COVID-19 pandemic on these habits in an adult population well known for its high prevalence of overweight and its associated chronic diseases in Brazil. Materials and Method: From May to July 2020, a digital survey was released, questioning about general health, diet and physical activity before and during decreed pandemic restrictions. Results: The majority (56%) of the 1739 respondents fitted the WHO classification criteria for overweight and obesity, 42% reported chronic morbidities and increased body weight since March 2020 (48%). The number of people not practicing any physical exercise had doubled in only three months (from 25% to 48% after March 2020) and time spend sedentary at work (38%) as well as in work-free times had increased (76%). Alimentation routines adapted partly worrisome habits like introducing more vespertine snacks between main meals but also positive changes like cooking at home (53%), and higher consumption of natural products (34%). Conclusion: Considering the age distribution of the participants (67% < 40 years of age), access to digital media, high educational level (77% with university degree), good to excellent basic sanitation (97%), the observed habit changes in only three months are concerning. It shows that even socially privileged people struggle to adapt healthy routines in times of crisis

Chronic Overexpression of Bradykinin in Kidney Causes Polyuria and Cardiac Hypertrophy

Acute intra-renal infusion of bradykinin increases diuresis and natriuresis via inhibition of vasopressin activity. However, the consequences of chronically increased bradykinin in the kidneys have not yet been studied. A new transgenic animal model producing an excess of bradykinin by proximal tubular cells (KapBK rats) was generated and submitted to different salt containing diets to analyze changes in blood pressure and other cardiovascular parameters, urine excretion, and composition, as well as levels and expression of renin-angiotensin system components. Despite that KapBK rats excrete more urine and sodium, they have similar blood pressure as controls with the exception of a small increase in systolic blood pressure (SBP). However, they present decreased renal artery blood flow, increased intrarenal expression of angiotensinogen, and decreased mRNA expression of vasopressin V1A receptor (AVPR1A), suggesting a mechanism for the previously described reduction of renal vasopressin sensitivity by bradykinin. Additionally, reduced heart rate variability (HRV), increased cardiac output and frequency, and the development of cardiac hypertrophy are the main chronic effects observed in the cardiovascular system. In conclusion: (1) the transgenic KapBK rat is a useful model for studying chronic effects of bradykinin in kidney; (2) increased renal bradykinin causes changes in renin angiotensin system regulation; (3) decreased renal vasopressin sensitivity in KapBK rats is related to decreased V1A receptor expression; (4) although increased renal levels of bradykinin causes no changes in mean arterial pressure (MAP), it causes reduction in HRV, augmentation in cardiac frequency and output and consequently cardiac hypertrophy in rats after 6 months of age

Physiological role of prolylcarboxypeptidase

Prolylcarboxypeptidase (PRCP, EC3.4.16.2) ist ein ubiquitär exprimiertes Enzym, mit höchster Expression im Maushirn. Es spaltet spezifisch die letzte carboxyterminale Aminosäure von Substraten, deren vorletzte Aminosäure ein Prolin ist. Seine bisher publizierten Substrate Angiotensin II (AngII) und alpha Melanocortin Stimulierendes Hormone (alphaMSH) legen eine Rolle von PRCP in der Entwicklung von kardiovaskulären und metabolischen Krankheiten nahe. Um die in vivo Funktion von PRCP zu studieren, wurde eine Knockout Maus generiert (PRCP-/-). Metabolischer Phänotyp: PRCP-/- Mäuse zeigten generell ein reduziertes Körpergewicht, selbst wenn sie über Monate mit einer Hochfettdiät versorgt wurden. Erhöhte Plasmaleptin Werte und Proopiomelanocortin (pomc) Expression in knockout Hypothalami wiesen auf eine wichtige Rolle von PRCP in der Regulation von Futteraufnahme und Energiehomöostase hin. Eines der Genprodukte von pomc ist alphaMSH, welches im Hypothalamus die Futteraufnahme terminiert. Die carboxyterminale Struktur dieses Neuropeptids erfüllt alle Voraussetzungen, um von PRCP gespalten zu werden. Zudem konnte prcp Promotoraktivität in den selben Hirnstrukturen gezeigt werden, in denen auch alphaMSH-Wirkung beschrieben wurde. Eine mögliche Funktion von PRCP wäre somit die Inaktivierung des Appetitzüglers alphaMSH im Hypothalamus. Kardiovasculärer Phänotyp: Zunächst erwiesen sich zirkulierende Ang-Peptide in PRCP-/- Mäusen als unverändert. Jedoch konnte ein erhöhtes Niveau des Degradationsproduktes Ang1-7 in der Niere gezeigt werden. Die Entdeckung einer erhöhten Enzymaktivität von Angiotensin Converting Enzyme 2 (ACE2) in PRCP-/- Nieren, wurde als Kompensation der fehlenden PRCP Aktivität in PRCP-/- Nieren interpretiert. bot einen Erklärungsansatz für dieses Ergebnisse. Es wird davon ausgegangen, daß ACE2 die fehlende PRCP Aktivität in knockout Mäusen kompensiert. Das es sich hierbei um eine lokale begrenzte Kompensation handeln muß, zeigten der erhöhte Blutdruck und Herzrate, sowie die milde Herzhypertrophie. Da spezifische prcp Promotoraktivität in Hirnnuclei gefunden wurde, die in die Kontrolle der Herzfrequenz und des Blutdrucks involviert sind, wird eine regulatorische Funktion von Hirnstamm-PRCP auf Herzrhytmus und Blutdruck vermutet.Prolylcarboxypeptidase (PRCP, EC3.4.16.2) is an enzyme specifically cleaving the last carboxy-terminal amino acid from substrates containing a penultimate proline. Its known potential substrates are linked to cardiovascular and metabolic phenomenon. To analyse the in vivo function of this enzyme a PRCP knockout mouse was generated. Homozygous knockout mice are viable but show tendency of decreased life span. In mice prcp expression is present in all tissues tested with very specific localizations of prcp promotor activity to distinct brain areas within the cortex, hippocampus, hypothalamus and the brain stem. The metabolic phenotype of PRCP deficient mice is characterized by low body weight even when feeding the animals a high fat diet. The increased plasma leptin levels and elevated expression of proopiomelanocortin gene (pomc) found in knockout hypothalami suggests an involvement of PRCP in the regulation of food intake and energy homeostasis. One of the gene products of pomc is alpha-melanocortin stimulating hormone (alphaMSH) that is terminating feeding when released from hypothalamic POMC neurons. Its carboxy-terminal structure is fitting the cleavage preferences of PRCP. Prcp promotor activities are localized in arcuate nucleus and paraventricular nucleus, brain areas of known alphaMSH signalling, supporting a role of PRCP in the degradation of central alphaMSH. The impact of PRCP on angiotensin II (AngII) metabolism was studied by determining the level of AngII and its degradation product Ang1-7 in blood and tissues. But instead of increased AngII levels due to the missing degradation enzyme in knockout mice, Ang1-7 levels were increased in kidney. These results were explainable by the increased activity of angiotensin converting enzyme 2 (ACE2) found in kidney. Probably ACE2 is compensating the lack of PRCP in the knockout mouse. Nevertheless, blood pressure and heart rate of PRCP knockout mice was increased. The mild hypertension was accompanied by mild hypertrophy of the hearts. Prcp promotor activity was found in brain stem an area important for regulation of blood pressure and heart rate suggesting that central PRCP regulates blood pressure

Polimorfismos genéticos do fator neurotrófico ciliar e relação com o peso corporal

Este trabalho tem como objetivo apresentar evidências com relação aos polimorfismos dos genes CNTF e CNTFR e o peso corporal, a partir dos dados encontrados na condução de uma revisão sistemática da literatura

Chronic Overexpression of Bradykinin in Kidney Causes Polyuria and Cardiac Hypertrophy

Acute intra-renal infusion of bradykinin increases diuresis and natriuresis via inhibition of vasopressin activity. However, the consequences of chronically increased bradykinin in the kidneys have not yet been studied. A new transgenic animal model producing an excess of bradykinin by proximal tubular cells (KapBK rats) was generated and submitted to different salt containing diets to analyze changes in blood pressure and other cardiovascular parameters, urine excretion, and composition, as well as levels and expression of renin-angiotensin system components. Despite that KapBK rats excrete more urine and sodium, they have similar blood pressure as controls with the exception of a small increase in systolic blood pressure (SBP). However, they present decreased renal artery blood flow, increased intrarenal expression of angiotensinogen, and decreased mRNA expression of vasopressin V1A receptor (AVPR1A), suggesting a mechanism for the previously described reduction of renal vasopressin sensitivity by bradykinin. Additionally, reduced heart rate variability (HRV), increased cardiac output and frequency, and the development of cardiac hypertrophy are the main chronic effects observed in the cardiovascular system. In conclusion: (1) the transgenic KapBK rat is a useful model for studying chronic effects of bradykinin in kidney; (2) increased renal bradykinin causes changes in renin angiotensin system regulation; (3) decreased renal vasopressin sensitivity in KapBK rats is related to decreased V1A receptor expression; (4) although increased renal levels of bradykinin causes no changes in mean arterial pressure (MAP), it causes reduction in HRV, augmentation in cardiac frequency and output and consequently cardiac hypertrophy in rats after 6 months of age

Metabolic pathways of Ang peptides.

<p>Metabolic routes of Ang I and II by neurolysin and other peptidases of the RAS. ACE =  angiotensin-converting enzyme, dipeptidyl carboxypeptidase I, Kininase II, EC 3.4.15.1, CD143; ACE-2 =  angiotensin-converting enzyme-2, EC 3.4.17.23; APA =  aminopeptidase A, glutamyl aminopeptidase, EC 3.4.11.7, CD249; NEP =  neprilysin, neutral endopeptidase, EC 3.4.24.11; PRCP =  prolyl carboxypeptidase, angiotensinase C, carboxypeptidase P, EC 3.4.16.2; PREP =  prolyl endopeptidase, post-prolyl cleaving enzyme, EC 3.4.21.26; TOP =  thimet oligopeptidase, EC 3.4.24.15. Adapted from Wright et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0105762#pone.0105762-Wright1" target="_blank">[12]</a>.</p

Histology WT1 WT2 KO1 KO2

<p>These files include autoradiographic films and histology files in .tiff format at 1200 dpi. These items were used to create the data shown in our manuscript. The nomenclature used for each animal (WT vs KO, -1, -2, -3, -4, 5) is described within the manuscript. We analyzed these files using MCID Image Analysis Software suite (http://www.mcid.co.uk/). Please warned that the files are large.</p

Autoradiographic film with KO1 and WT2

<p>These files include autoradiographic films and histology files in .tiff format at 1200 dpi. These items were used to create the data shown in our manuscript. The nomenclature used for each animal (WT vs KO, -1, -2, -3, -4, 5) is described within the manuscript. We analyzed these files using MCID Image Analysis Software suite (http://www.mcid.co.uk/). Please warned that the files are large.</p

Histology WT3 KO3

<p>These files include autoradiographic films and histology files in .tiff format at 1200 dpi. These items were used to create the data shown in our manuscript. The nomenclature used for each animal (WT vs KO, -1, -2, -3, -4, 5) is described within the manuscript. We analyzed these files using MCID Image Analysis Software suite (http://www.mcid.co.uk/). Please warned that the files are large.</p