scholarly journals Insects as a New Complex Model in Hormonal Basis of Obesity

2021 ◽  
Vol 22 (20) ◽  
pp. 11066
Author(s):  
Karolina Walkowiak-Nowicka ◽  
Szymon Chowański ◽  
Arkadiusz Urbański ◽  
Paweł Marciniak
Keyword(s):  
Signaling Pathways ◽  
Complex Model ◽  
Endocrine Regulation ◽  
Human Obesity ◽  
Ideal Model ◽  
Obesity Epidemic ◽  
Disease Occurrence ◽  
Hormonal Balance ◽  
Pathways Analysis ◽  
Physiological Analysis

Nowadays, one of the biggest problems in healthcare is an obesity epidemic. Consumption of cheap and low-quality energy-rich diets, low physical activity, and sedentary work favor an increase in the number of obesity cases within many populations/nations. This is a burden on society, public health, and the economy with many deleterious consequences. Thus, studies concerning this disorder are extremely needed, including searching for new, effective, and fitting models. Obesity may be related, among other factors, to disrupting adipocytes activity, disturbance of metabolic homeostasis, dysregulation of hormonal balance, cardiovascular problems, or disorders in nutrition which may lead to death. Because of the high complexity of obesity, it is not easy to find an ideal model for its studies which will be suitable for genetic and physiological analysis including specification of different compounds’ (hormones, neuropeptides) functions, as well as for signaling pathways analysis. In recent times, in search of new models for human diseases there has been more and more attention paid to insects, especially in neuro-endocrine regulation. It seems that this group of animals might also be a new model for human obesity. There are many arguments that insects are a good, multidirectional, and complex model for this disease. For example, insect models can have similar conservative signaling pathways (e.g., JAK-STAT signaling pathway), the presence of similar hormonal axis (e.g., brain–gut axis), or occurrence of structural and functional homologues between neuropeptides (e.g., neuropeptide F and human neuropeptide Y, insulin-like peptides, and human insulin) compared to humans. Here we give a hint to use insects as a model for obesity that can be used in multiple ways: as a source of genetic and peptidomic data about etiology and development correlated with obesity occurrence as well as a model for novel hormonal-based drug activity and their impact on mechanism of disease occurrence.

scholarly journals Endospanin 1 Determines the Balance of Leptin-Regulated Hypothalamic Functions

2018 ◽  
Vol 108 (2) ◽  
pp. 132-141
Author(s):  
Clara Roujeau ◽  
Ralf Jockers ◽  
Julie Dam
Keyword(s):  
Signaling Pathways ◽  
Intracellular Trafficking ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Human Obesity ◽  
Leptin Signaling ◽  
Diet Induced Obesity ◽  
Important Regulator ◽  
Neuronal Plasma Membrane ◽  
Underlying Mechanisms

Endospanin 1 (Endo1), a protein encoded in humans by the same gene than the leptin receptor (ObR), and increased by diet-induced obesity, is an important regulator of ObR trafficking and cell surface exposure, determining leptin signaling strength. Defective intracellular trafficking of the leptin receptor to the neuronal plasma membrane has been proposed as a mechanism underlying the development of leptin resistance observed in human obesity. More recently, Endo1 has emerged as a mediator of “selective leptin resistance.” The underlying mechanisms of the latter are not completely understood, but the possibility of differential activation of leptin signaling pathways was suggested among others. In this respect, the expression level of Endo1 is crucial for the appropriate balance between different leptin signaling pathways and leptin functions in the hypothalamus and is likely participating in selective leptin resistance for the control of energy and glucose homeostasis.

Mapping multiple drivers of human obesity

2017 ◽  
Vol 40 ◽  
Author(s):  
R. Alexander Bentley ◽  
Michael J. O'Brien
Keyword(s):  
Social Influence ◽  
Alternative Explanation ◽  
Human Obesity ◽  
Sugar Sweetened Beverages ◽  
Obesity Epidemic ◽  
Insurance Hypothesis ◽  
High Sugar ◽  
Reasonable Explanation ◽  
Sweetened Beverages

AbstractThe insurance hypothesis is a reasonable explanation for the current obesity epidemic. One alternative explanation is that the marketing of high-sugar foods, especially sugar-sweetened beverages, drives the rise in obesity. Another prominent hypothesis is that obesity spreads through social influence. We offer a framework for estimating the extent to which these different models explain the rise in obesity.

scholarly journals Comparative transcriptional analysis provides insights of possible molecular mechanisms of wing polyphenism induced by postnatal crowding in Aphis gossypii

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Jichao JI ◽  
Shuai ZHANG ◽  
Junyu LUO ◽  
Li WANG ◽  
Xiangzhen ZHU ◽  
...  
Keyword(s):  
Population Density ◽  
Signaling Pathways ◽  
Differentially Expressed Genes ◽  
Molecular Mechanisms ◽  
Aphis Gossypii ◽  
Plant Viruses ◽  
Differentially Expressed ◽  
Transcriptional Analysis ◽  
Cotton Aphid ◽  
Pathways Analysis

Abstract Background Aphis gossypii is a worldwide sap-sucking pest with a variety of hosts and a vector of more than 50 plant viruses. The strategy of wing polyphenism, mostly resulting from population density increasing, contributes to the evolutionary success of this pest. However, the related molecular basis remains unclear. Here, we identified the effects of postnatal crowding on wing morph determination in cotton aphid, and examined the transcriptomic differences between wingless and wing morphs. Results Effect of postnatal crowding on wing determination in A. gossypii was evaluated firstly. Under the density of 5 nymphs·cm− 2, no wing aphids appeared. Proportion of wing morphs rised with the increase of density in a certain extent, and peaked to 56.1% at the density of 20 nymphs·cm− 2, and reduced afterwards. Then, transcriptomes of wingless and wing morphs were assembled and annotated separately to identify potentially exclusively or differentially expressed transcripts between these two morphs, in which 3 126 and 3 392 unigenes annotated in Nr (Non-redundant protein sequence) database were found in wingless or wing morphs exclusively. Moreover, 3 187 up- and 1 880 down-regulated genes were identified in wing versus wingless aphid. Pathways analysis suggested the involvement of differentially expressed genes in multiple cellular signaling pathways involved in wing morphs determination, including lipid catabolic and metabolism, insulin, ecdysone and juvenile hormone biosynthesis. The expression levels of related genes were validated by the reverse transcription quantitative real time polymerase chain reaction (RT-qPCR) soon afterwards. Conclusions The present study identified the effects of postnatal crowding on wing morphs induction and demonstrated that the critical population density for wing morphs formation in A. gossypii was 20 nymphs·cm− 2. Comparative transcriptome analysis provides transcripts potentially expressed exclusively in wingless or wing morph, respectively. Differentially expressed genes between wingless and wing morphs were identified and several signaling pathways potentially involved in cotton aphid wing differentiation were obtained.

scholarly journals Filamentation Regulatory Pathways Control Adhesion-Dependent Surface Responses in Yeast

Genetics ◽  
2019 ◽  
Vol 212 (3) ◽  
pp. 667-690 ◽  
Author(s):  
Jacky Chow ◽  
Izzy Starr ◽  
Sheida Jamalzadeh ◽  
Omar Muniz ◽  
Anuj Kumar ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Fungal Pathogens ◽  
Target Genes ◽  
Filamentous Growth ◽  
Surface Growth ◽  
Low Oxygen ◽  
Regulatory Pathways ◽  
Biological Responses ◽  
Pathways Analysis ◽  
Phenotype Analysis

Signaling pathways can regulate biological responses by the transcriptional regulation of target genes. In yeast, multiple signaling pathways control filamentous growth, a morphogenetic response that occurs in many species including fungal pathogens. Here, we examine the role of signaling pathways that control filamentous growth in regulating adhesion-dependent surface responses, including mat formation and colony patterning. Expression profiling and mutant phenotype analysis showed that the major pathways that regulate filamentous growth [filamentous growth MAPK (fMAPK), RAS, retrograde (RTG), RIM101, RPD3, ELP, SNF1, and PHO85] also regulated mat formation and colony patterning. The chromatin remodeling complex, SAGA, also regulated these responses. We also show that the RAS and RTG pathways coregulated a common set of target genes, and that SAGA regulated target genes known to be controlled by the fMAPK, RAS, and RTG pathways. Analysis of surface growth-specific targets identified genes that respond to low oxygen, high temperature, and desiccation stresses. We also explore the question of why cells make adhesive contacts in colonies. Cell adhesion contacts mediated by the coregulated target and adhesion molecule, Flo11p, deterred entry into colonies by macroscopic predators and impacted colony temperature regulation. The identification of new regulators (e.g., SAGA), and targets of surface growth in yeast may provide insights into fungal pathogenesis in settings where surface growth and adhesion contributes to virulence.

scholarly journals The meaning of sensitivity functions in signaling pathways analysis

2014 ◽  
Vol 19 (8) ◽  
pp. 2697-2707 ◽  
Author(s):  
Jaroslaw Smieja ◽  
◽  
Malgorzata Kardynska ◽  
Arkadiusz Jamroz ◽  
Keyword(s):  
Signaling Pathways ◽  
Sensitivity Functions ◽  
Pathways Analysis

scholarly journals Loss of Planar Cell Polarity Effector Fuzzy Causes Renal Hypoplasia by Disrupting Several Signaling Pathways

2021 ◽  
Vol 10 (1) ◽  
pp. 1
Author(s):  
Irene-Yanran Wang ◽  
Chen-Fang Chung ◽  
Sima Babayeva ◽  
Tamara Sogomonian ◽  
Elena Torban
Keyword(s):  
Signaling Pathways ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Primary Cilia ◽  
Branching Morphogenesis ◽  
Effector Proteins ◽  
Renal Hypoplasia ◽  
Developmental Disturbance ◽  
Pathways Analysis ◽  
Nephron Progenitor

In vertebrates, the planar cell polarity (PCP) pathway regulates tissue morphogenesis during organogenesis, including the kidney. Mutations in human PCP effector proteins have been associated with severe syndromic ciliopathies. Importantly, renal hypoplasia has been reported in some patients. However, the developmental disturbance that causes renal hypoplasia is unknown. Here, we describe the early onset of profound renal hypoplasia in mice homozygous for null mutation of the PCP effector gene, Fuzzy. We found that this phenotype is caused by defective branching morphogenesis of the ureteric bud (UB) in the absence of defects in nephron progenitor specification or in early steps of nephrogenesis. By using various experimental approaches, we show that the loss of Fuzzy affects multiple signaling pathways. Specifically, we found mild involvement of GDNF/c-Ret pathway that drives UB branching. We noted the deficient expression of molecules belonging to the Bmp, Fgf and Shh pathways. Analysis of the primary cilia in the UB structures revealed a significant decrease in ciliary length. We conclude that renal hypoplasia in the mouse Fuzzy mutants is caused by defective UB branching associated with dysregulation of ciliary and non-ciliary signaling pathways. Our work suggests a PCP effector-dependent pathogenetic mechanism that contributes to renal hypoplasia in mice and humans.

The Human Obesity Epidemic - A Physiological Perspective

2004 ◽  
Vol 4 (2) ◽  
pp. 91-104 ◽  
Author(s):  
K. Niswender ◽  
D. Clegg ◽  
C. Morrison ◽  
G. Morton ◽  
S. Benoit
Keyword(s):  
Human Obesity ◽  
Obesity Epidemic

Intricacies of the endothelin system in human obesity: role in the development of complications and potential as a therapeutic target

2020 ◽  
Vol 98 (9) ◽  
pp. 563-569 ◽  
Author(s):  
Francesca Schinzari ◽  
Carmine Cardillo
Keyword(s):  
Adipose Tissue ◽  
Vascular Dysfunction ◽  
Tissue Expansion ◽  
Human Obesity ◽  
Metabolic Complications ◽  
Perivascular Adipose Tissue ◽  
Obesity Epidemic ◽  
The Metabolic Syndrome ◽  
Obesity And Diabetes ◽  
Endothelin System

Activation of the vascular endothelin-1 (ET-1) system is a key abnormality in vascular dysfunction of human obesity, especially in patients developing complications, such as the metabolic syndrome, diabetes, and atherosclerosis. Vascular insulin resistance, an increased insulin-stimulated endothelial production of ET-1 combined with impaired nitric oxide availability, is the hallmark of obesity-related vasculopathy, but dysregulated adipokine release from obese adipose tissue may contribute to the predominance of ET-1-dependent vasoconstriction. ET-1, in turn, might determine unhealthy obese adipose tissue expansion, with visceral and perivascular adipose tissue changes driving the release of inflammatory cytokines and atherogenic chemokines. In addition, ET-1 might also play a role in the development of the metabolic complications of obesity. Studies have shown inhibition of lipoprotein lipase activity by ET-1, with consequent hypertriglyceridemia. Also, ET-1 in pancreatic islets seems to contribute to beta cell dysfunction, hence affecting insulin production and development of diabetes. Moreover, ET-1 may play a role in nonalcoholic steatohepatitis. Recent clinical trials using innovative design have demonstrated that antagonism of ET-type A receptors protects against some complications of obesity and diabetes, such as nephropathy. These findings encourage further investigation to evaluate whether targeting the ET-1 system could afford better protection against other consequences of the obesity epidemic.

scholarly journals Transgenerational Obesity and Healthy Aging in Drosophila

2019 ◽  
Vol 74 (10) ◽  
pp. 1582-1589 ◽  
Author(s):  
Tara-Lyn Camilleri-Carter ◽  
Damian K Dowling ◽  
Rebecca L. Robker ◽  
Matthew D W Piper
Keyword(s):  
Metabolic Pathways ◽  
Healthy Aging ◽  
Fruit Fly ◽  
Dietary Interventions ◽  
Ideal Model ◽  
Substantial Evidence ◽  
Obesity Epidemic ◽  
Age Related ◽  
Nutrient Signaling ◽  
Nutritional Effects

Abstract Substantial evidence suggests that individuals born to overweight and obese parents suffer detrimental health consequences that dramatically decrease healthy aging. The number of obese individuals worldwide now exceeds the number of under- and malnourished individuals. This obesity epidemic is responsible for approximately 4 million deaths worldwide each year, and predisposes sufferers to a range of age-related diseases such as cardiovascular diseases, and metabolic syndrome. Additionally, obesity is associated with an accelerated onset of age-related ailments, such as cancers and inflammation. The importance of dietary interventions to reduce the incidence of obesity is magnified by emerging evidence that parental physiology can predispose future generations to poor health outcomes. Characterizing and understanding these effects, and how they are mediated, is important if we are to continue to drive improvements to population health. In this article, we synthesize evidence for the intergenerational and transgenerational phenotypic effects of parental obesity. We concentrate on how the fruit fly Drosophila melanogaster can be used as a model to study these effects. Fruit flies are highly tractable, and their conserved nutrient signaling and metabolic pathways make them an ideal model for studying nutritional effects on metabolic, reproductive, and aging phenotypes.

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