scholarly journals Fat Body—Multifunctional Insect Tissue

Insects ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 547
Author(s):  
Patrycja Skowronek ◽  
Łukasz Wójcik ◽  
Aneta Strachecka

The biodiversity of useful organisms, e.g., insects, decreases due to many environmental factors and increasing anthropopressure. Multifunctional tissues, such as the fat body, are key elements in the proper functioning of invertebrate organisms and resistance factors. The fat body is the center of metabolism, integrating signals, controlling molting and metamorphosis, and synthesizing hormones that control the functioning of the whole body and the synthesis of immune system proteins. In fat body cells, lipids, carbohydrates and proteins are the substrates and products of many pathways that can be used for energy production, accumulate as reserves, and mobilize at the appropriate stage of life (diapause, metamorphosis, flight), determining the survival of an individual. The fat body is the main tissue responsible for innate and acquired humoral immunity. The tissue produces bactericidal proteins and polypeptides, i.e., lysozyme. The fat body is also important in the early stages of an insect’s life due to the production of vitellogenin, the yolk protein needed for the development of oocytes. Although a lot of information is available on its structure and biochemistry, the fat body is an interesting research topic on which much is still to be discovered.

1959 ◽  
Vol 197 (2) ◽  
pp. 360-366 ◽  
Author(s):  
Herbert C. Dessauer ◽  
Wade Fox

The first stage of follicle development was due chiefly to hydration; during the second (deutoplasmic) stage 60 mg of solid were taken up with each 100 mg increase in follicle weight. Plasma calcium and protein P rose near end of hydration stage, remained elevated during deutoplasmic stage, reached extreme levels (max. Ca = 90 mm/l.; protein P = 86 mm/l.) near ovulation, and generally fell to anestrous levels while eggs were in early cleavage. Calcium increased in proportion to protein bound P of both plasma and follicles. During deutoplasmic stage a phospho-lipoprotein, of similar gross composition to yolk protein, appeared in plasma. Liver weight increased during hydration stage, remained elevated throughout deutoplasmic stage and decreased near ovulation. Fat body weight increased with onset of estrus, reached maximum during hydration stage and progressively decreased during deutoplasmic stage. Plasma and liver changes characteristic of estrus were reproduced in fasted male snakes with estradiol injections.


2021 ◽  
Author(s):  
Ye Yin ◽  
Yangyang Wu ◽  
Xu Zhang ◽  
Yeting Zhu ◽  
Yue Sun ◽  
...  

<a>Downregulation of mitochondrial function in adipose tissue is considered as one important driver for the development of obesity-associated metabolic disorders. Inorganic Pyrophosphatase 1 (PPA1) is an enzyme catalyzes the hydrolysis of PPi to Pi, and is required for anabolism to take place in cells. Although alternation of PPA1 has been related to some diseases, the importance of PPA1 in metabolic syndromes has never been discussed before. In this study, we found that global PPA1 knockout mice (PPA1<sup>+/-</sup>) showed impaired glucose tolerance and severe insulin resistance under HFD feeding. In addition, impaired adipose tissue development and ectopic lipid accumulation were also observed. Conversely, overexpression of PPA1 in adipose tissue by AAV injection can partly reverse the metabolic disorders in PPA1<sup>+/-</sup> mice, suggesting that impaired adipose tissue function is responsible for the metabolic disorders observed in PPA1<sup>+/- </sup>mice. Mechanistic studies revealed that PPA1 acted as a PPARγ target gene to maintain mitochondrial function in adipocytes. Furthermore, specific knockdown of PPA1 in fat body of <i>Drosophila</i> led to impaired mitochondria morphology, decreased lipid storage, and made <i>Drosophila</i> more sensitive to starvation. In conclusion, for the first time, our findings demonstrated the importance of PPA1 in maintaining adipose tissue function and whole body metabolic homeostasis.</a>


2020 ◽  
Author(s):  
Tatyana Dobreva ◽  
David Brown ◽  
Jong Hwee Park ◽  
Matt Thomson

AbstractAn individual’s immune system is driven by both genetic and environmental factors that vary over time. To better understand the temporal and inter-individual variability of gene expression within distinct immune cell types, we developed a platform that leverages multiplexed single-cell sequencing and out-of-clinic capillary blood extraction to enable simplified, cost-effective profiling of the human immune system across people and time at single-cell resolution. Using the platform, we detect widespread differences in cell type-specific gene expression between subjects that are stable over multiple days.SummaryIncreasing evidence implicates the immune system in an overwhelming number of diseases, and distinct cell types play specific roles in their pathogenesis.1,2 Studies of peripheral blood have uncovered a wealth of associations between gene expression, environmental factors, disease risk, and therapeutic efficacy.4 For example, in rheumatoid arthritis, multiple mechanistic paths have been found that lead to disease, and gene expression of specific immune cell types can be used as a predictor of therapeutic non-response.12 Furthermore, vaccines, drugs, and chemotherapy have been shown to yield different efficacy based on time of administration, and such findings have been linked to the time-dependence of gene expression in downstream pathways.21,22,23 However, human immune studies of gene expression between individuals and across time remain limited to a few cell types or time points per subject, constraining our understanding of how networks of heterogeneous cells making up each individual’s immune system respond to adverse events and change over time.


2019 ◽  
Vol 3 ◽  
pp. 147 ◽  
Author(s):  
Lucy A. Oakey ◽  
Rachel S. Fletcher ◽  
Yasir S. Elhassan ◽  
David M. Cartwright ◽  
Craig L. Doig ◽  
...  

Background: Skeletal muscle is central to whole body metabolic homeostasis, with age and disease impairing its ability to function appropriately to maintain health. Inadequate NAD+ availability is proposed to contribute to pathophysiology by impairing metabolic energy pathway use. Despite the importance of NAD+ as a vital redox cofactor in energy production pathways being well-established, the wider impact of disrupted NAD+ homeostasis on these pathways is unknown. Methods: We utilised skeletal muscle myotube models to induce NAD+ depletion, repletion and excess and conducted metabolic tracing to provide comprehensive and detailed analysis of the consequences of altered NAD+ metabolism on central carbon metabolic pathways. We used stable isotope tracers, [1,2-13C] D-glucose and [U-13C] glutamine, and conducted combined 2D-1H,13C-heteronuclear single quantum coherence (HSQC) NMR spectroscopy and GC-MS analysis. Results: NAD+ excess driven by nicotinamide riboside (NR) supplementation within skeletal muscle cells resulted in enhanced nicotinamide clearance, but had no effect on energy homeostasis or central carbon metabolism. Nicotinamide phosphoribosyltransferase (NAMPT) inhibition induced NAD+ depletion and resulted in equilibration of metabolites upstream of glyceraldehyde phosphate dehydrogenase (GAPDH). Aspartate production through glycolysis and TCA cycle activity was increased in response to low NAD+, which was rapidly reversed with repletion of the NAD+ pool using NR. NAD+ depletion reversibly inhibits cytosolic GAPDH activity, but retains mitochondrial oxidative metabolism, suggesting differential effects of this treatment on sub-cellular pyridine pools. When supplemented, NR efficiently reversed these metabolic consequences. However, the functional relevance of increased aspartate levels after NAD+ depletion remains unclear, and requires further investigation. Conclusions: These data highlight the need to consider carbon metabolism and clearance pathways when investigating NAD+ precursor usage in models of skeletal muscle physiology.


Vaccines ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 636 ◽  
Author(s):  
Rossella Cianci ◽  
Laura Franza ◽  
Maria Grazia Massaro ◽  
Raffaele Borriello ◽  
Francesco De Vito ◽  
...  

Vaccinations are among the most effective medical procedures and have had an incredible impact on almost everyone’s life. One of the populations that can benefit the most from them are elderly people. Unfortunately, in this group, vaccines are less effective than in other groups, due to immunosenescence. The immune system ages like the whole body and becomes less effective in responding to infections and vaccinations. At the same time, immunosenescence also favors an inflammatory microenvironment, which is linked to many conditions typical of the geriatrics population. The microbiota is one of the key actors in modulating the immune response and, in this review, we discuss the current evidence on the role of microbiota in regulating the immune response to vaccines, particularly in elderly people.


2019 ◽  
Vol 32 (1) ◽  
pp. 128-145 ◽  
Author(s):  
Sabrina Campisano ◽  
Anabela La Colla ◽  
Stella M. Echarte ◽  
Andrea N. Chisari

AbstractEarly-life nutrition plays a critical role in fetal growth and development. Food intake absence and excess are the two main types of energy malnutrition that predispose to the appearance of diseases in adulthood, according to the hypothesis of ‘developmental origins of health and disease’. Epidemiological data have shown an association between early-life malnutrition and the metabolic syndrome in later life. Evidence has also demonstrated that nutrition during this period of life can affect the development of the immune system through epigenetic mechanisms. Thus, epigenetics has an essential role in the complex interplay between environmental factors and genetics. Altogether, this leads to the inflammatory response that is commonly seen in non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome. In conjunction, DNA methylation, covalent modification of histones and the expression of non-coding RNA are the epigenetic phenomena that affect inflammatory processes in the context of NAFLD. Here, we highlight current understanding of the mechanisms underlying developmental programming of NAFLD linked to epigenetic modulation of the immune system and environmental factors, such as malnutrition.


2020 ◽  
Vol 9 (3) ◽  
pp. 249-262
Author(s):  
Xiaochang Liu ◽  
Zheng Liu ◽  
Duo Wang ◽  
Yang Han ◽  
Sai Hu ◽  
...  

Abstract Whole-body exposure to low-dose radiation due to diagnostic imaging procedures, occupational hazards and radiation accidents is a source of concern. In this study, we analyzed the effects of single and long-term low-dose irradiation on the immune system. Male Balb/c mice received a single whole-body dose of irradiation (0.01, 0.05, 0.2, 0.5 or 1 Gy). For long-term irradiation, mice were irradiated 10 times (total dose of 0.2, 0.5 or 1 Gy) over a period of 6 weeks. Two days after single or long-term irradiation, the numbers of splenic macrophages, natural killer cells and dendritic cells were reduced, and the spleen organ coefficient was decreased. At 2 Days after long-term low-dose irradiation, the number of white blood cells in the peripheral blood of the mice decreased. Between 7 and 14 Days after long-term low-dose irradiation, the number of immune cells in the thymus and spleen began to increase and then stabilized. Th1/Th2 cytokines and reactive oxygen species-related proteins first decreased and then increased to a plateau. Our results show a significant difference in the effects of single and long-term low-dose irradiation on the immune system.


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