scholarly journals Angiogenin mediates paternal inflammation-induced metabolic disorders in offspring through sperm tsRNAs

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yanwen Zhang ◽  
Li Ren ◽  
Xiaoxiao Sun ◽  
Zhilong Zhang ◽  
Jie Liu ◽  
...  

AbstractPaternal environmental inputs can influence various phenotypes in offspring, presenting tremendous implications for basic biology and public health and policy. However, which signals function as a nexus to transmit paternal environmental inputs to offspring remains unclear. Here we show that offspring of fathers with inflammation exhibit metabolic disorders including glucose intolerance and obesity. Deletion of a mouse tRNA RNase, Angiogenin (Ang), abolished paternal inflammation-induced metabolic disorders in offspring. Additionally, Ang deletion prevented the inflammation-induced alteration of 5′-tRNA-derived small RNAs (5′-tsRNAs) expression profile in sperm, which might be essential in composing a sperm RNA ‘coding signature’ that is needed for paternal epigenetic memory. Microinjection of sperm 30–40 nt RNA fractions (predominantly 5′-tsRNAs) from inflammatory Ang+/+ males but not Ang–/– males resulted in metabolic disorders in the resultant offspring. Moreover, zygotic injection with synthetic 5′-tsRNAs which increased in inflammatory mouse sperm and decreased by Ang deletion partially resembled paternal inflammation-induced metabolic disorders in offspring. Together, our findings demonstrate that Ang-mediated biogenesis of 5′-tsRNAs in sperm contributes to paternal inflammation-induced metabolic disorders in offspring.

PEDIATRICS ◽  
1981 ◽  
Vol 67 (3) ◽  
pp. 443-443
Author(s):  
George E. Porter

We have had an interesting experience in our office where we do routine ferric chloride tests on our newborn infants as well as a check for glucose at the time of their first visit. We recently came up with a positive ferric chloride test on a child's diaper. Urine was collected and sent to the Metabolic Disorders Laboratory at the Massachusetts Department of Public Health State Laboratory in Jamaica Plain; test results were normal. Results of tests performed at the time of the child's birth were also normal.


DNA Research ◽  
2012 ◽  
Vol 20 (2) ◽  
pp. 109-125 ◽  
Author(s):  
M. Hackenberg ◽  
P.-J. Huang ◽  
C.-Y. Huang ◽  
B.-J. Shi ◽  
P. Gustafson ◽  
...  

2020 ◽  
Vol 11 (3) ◽  
pp. 477-482
Author(s):  
Shokreya Ehsani ◽  
Pouriya Darabiyan ◽  
Kourosh Zarea ◽  
Saeed Ghanbari ◽  
Aseya Temori

Introduction: Diabetes is one of the most common metabolic disorders and is one of the top 10 leading causes of death in adults. Therefore, this study was conducted to investigate the epidemiological prevalence of diabetes in Afghanistan between 2015 and 2019. Methods: This descriptive cross-sectional study was performed using the information of diabetics registered in the system related to the Ministry of Health of Afghanistan from 2015 to 2019. Eventually, people's information, including age, gender, and place of residence, was entered into STATA software version 12 and analyzed using descriptive statistics tests. Results: The study, which was performed on 49,332 people with diabetes in 34 provinces and 8 regions of Afghanistan, found that most of the female studied were 55.2% (27,231) female and had the highest and lowest prevalence in the region. The order is related to South East and South. The average prevalence of diabetes per 10,000 people is about 62.13. Conclusions: The prevalence of diabetes in Afghanistan over a five-year period in men and women is on the rise, requiring more attention from relevant authorities to improve public health and prevent, control and treat chronic diseases such as diabetes.


2018 ◽  
Vol 9 (12) ◽  
pp. 6165-6178 ◽  
Author(s):  
Joris Vidé ◽  
Béatrice Bonafos ◽  
Gilles Fouret ◽  
Melha Benlebna ◽  
Joël Poupon ◽  
...  

The prevalence of metabolic syndrome components, such as obesity, glucose intolerance and hepatic steatosis, is rapidly increasing and becoming a major issue of public health.


PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0177275 ◽  
Author(s):  
Farzaneh Assadian ◽  
Wael Kamel ◽  
Göran Laurell ◽  
Catharina Svensson ◽  
Tanel Punga ◽  
...  

2021 ◽  
Vol 22 (15) ◽  
pp. 7995
Author(s):  
Jianfeng Du ◽  
Yu Tina Zhao ◽  
Hao Wang ◽  
Ling X. Zhang ◽  
Gangjian Qin ◽  
...  

Regulated/activated protein kinase (PRAK) plays a crucial role in modulating biological function. However, the role of PRAK in mediating cardiac dysfunction and metabolic disorders remains unclear. We examined the effects of deletion of PRAK on modulating cardiac function and insulin resistance in mice exposed to a high-fat diet (HFD). Wild-type and PRAK−/− mice at 8 weeks old were exposed to either chow food or HFD for a consecutive 16 weeks. Glucose tolerance tests and insulin tolerance tests were employed to assess insulin resistance. Echocardiography was employed to assess myocardial function. Western blot was used to determine the molecular signaling involved in phosphorylation of IRS-1, AMPKα, ERK-44/42, and irisin. Real time-PCR was used to assess the hypertrophic genes of the myocardium. Histological analysis was employed to assess the hypertrophic response, interstitial myocardial fibrosis, and apoptosis in the heart. Western blot was employed to determine cellular signaling pathway. HFD-induced metabolic stress is indicated by glucose intolerance and insulin intolerance. PRAK knockout aggravated insulin resistance, as indicated by glucose intolerance and insulin intolerance testing as compared with wild-type littermates. As compared with wild-type mice, hyperglycemia and hypercholesterolemia were manifested in PRAK-knockout mice following high-fat diet intervention. High-fat diet intervention displayed a decline in fractional shortening and ejection fraction. However, deletion of PRAK exacerbated the decline in cardiac function as compared with wild-type mice following HFD treatment. In addition, PRAK knockout mice enhanced the expression of myocardial hypertrophic genes including ANP, BNP, and βMHC in HFD treatment, which was also associated with an increase in cardiomyocyte size and interstitial fibrosis. Western blot indicated that deletion of PRAK induces decreases in phosphorylation of IRS-1, AMPKα, and ERK44/42 as compared with wild-type controls. Our finding indicates that deletion of PRAK promoted myocardial dysfunction, cardiac remodeling, and metabolic disorders in response to HFD.


2009 ◽  
Vol 94 (6) ◽  
pp. 1853-1878 ◽  
Author(s):  
Sherita H. Golden ◽  
Karen A. Robinson ◽  
Ian Saldanha ◽  
Blair Anton ◽  
Paul W. Ladenson

Abstract Context: There has not been a comprehensive compilation of data regarding the epidemiology of all endocrine and metabolic disorders in the United States. Evidence Acquisition: We included 54 disorders with clinical and public health significance. We identified population-based studies that provided U.S. prevalence and/or incidence data by searching PubMed in December 2007 for English-language reports, hand-searching reference lists of six textbooks of endocrinology, obtaining additional resources from identified experts in each subspecialty, and searching epidemiological databases and web sites of relevant organizations. When available, we selected articles with data from 1998 or later. Otherwise, we selected the article with the most recent data, broadest geographical coverage, and most stratifications by sex, ethnicity, and/or age. Ultimately, we abstracted data from 70 articles and 40 cohorts. Evidence Synthesis: Endocrine disorders with U.S. prevalence estimates of at least 5% in adults included diabetes mellitus, impaired fasting glucose, impaired glucose tolerance, obesity, metabolic syndrome, osteoporosis, osteopenia, mild-moderate hypovitaminosis D, erectile dysfunction, dyslipidemia, and thyroiditis. Erectile dysfunction and osteopenia/osteoporosis had the highest incidence in males and females, respectively. The least prevalent conditions, affecting less than 1% of the U.S. population, were diabetes mellitus in children and pituitary adenoma. Conditions with the lowest incidence were adrenocortical carcinoma, pheochromocytoma, and pituitary adenomas. Certain disorders, such as hyperparathyroidism and thyroid disorders, were more common in females. As expected, the prevalence of diabetes mellitus was highest among ethnic minorities. Sparse data were available on pituitary, adrenal, and gonadal disorders. Conclusions: The current review shows high prevalence and incidence of common endocrine and metabolic disorders. Defining the epidemiology of these conditions will provide clues to risk factors and identify areas to allocate public health and research resources.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Hayashi ◽  
I Shimizu ◽  
Y Yoshida ◽  
G Katsuumi ◽  
M Suda ◽  
...  

Abstract   The prevalence of obesity is increasing worldwide. Obese individuals are predisposed to cardio-metabolic disorders. Brown adipose tissue (BAT) is an active metabolic organ abundant with mitochondria, and studies suggest a potential role of BAT in the maintenance of metabolic health in rodents and humans. Metabolic stress causes BAT dysfunction, but the underlying mechanisms are largely unknown. Coagulation factor Xa (FXa) is critically involved in a coagulation cascade, and it is also known to mediate biological effects by the activation of protease-activated receptor (PAR)-signaling. Accumulating evidence shows that PAR1 contributes to tissue remodeling in cardiovascular system. Analyzing deposited microarray data, we found transcripts for coagulation factors including factor VII (F7), factor X (F10), and PAR1 receptor were increased in BAT from obese mice. Here we show a previously unknown role of FXa-PAR signaling in promoting BAT dysfunction and systemic metabolic disorder in a murine dietary obese model. Imposing a high fat diet (HFD) on C57BL/6NCr mice led to a marked increase in tissue factor (TF), coagulation factor VII and FXa in BAT. TF-FVIIa (activated form of FVII)-FXa complex is known to activate PAR1, and we found a significant increase in PAR1 expression in BAT upon metabolic stress. Administration of a FXa inhibitor ameliorated BAT whitening, improved thermogenic response and systemic glucose intolerance upon dietary obesity. Fxa inhibition reduced reactive oxygen species (ROS) level in BAT. In contrast, administration of warfarin did not show any phenotype in BAT. BAT specific TF and PAR1 over-expression model showed significant whitening of this tissue, which was associated with systemic glucose intolerance. We generated BAT specific PAR1 KO mice. BAT-PAR1 KO mice exhibited re-browning of BAT along with reduced ROS level in this tissue. In BAT-PAR1 KO mice, glucose intolerance and thermogenic response under a metabolically stressed condition were ameliorated. In differentiated brown adipocytes, FXa markedly increased mitochondrial ROS and reduced mitochondrial membrane potential. Inhibition of PAR1 ameliorated FXa-induced mitochondrial ROS production and reduction in membrane potential. We also found that plasma FXa level did not increase in obese mice as well as in obese individuals. These results suggest the previously unknown role of coagulation systems in promoting BAT dysfunction, leading to systemic metabolic disorders. Maintenance of BAT homeostasis through the suppression of FXa-PAR1 signaling would become a new therapeutic target for obesity and diabetes. Funding Acknowledgement Type of funding source: None


Sign in / Sign up

Export Citation Format

Share Document