scholarly journals Insulin Signaling in the Peripheral and Central Nervous System Regulates Female Sexual Receptivity during Starvation in Drosophila

2017 ◽  
Vol 8 ◽  
Author(s):  
Sébastien Lebreton ◽  
Mikael A. Carlsson ◽  
Peter Witzgall

Endocrine ◽  
2001 ◽  
Vol 16 (3) ◽  
pp. 227-234 ◽  
Author(s):  
Maria Luiza de L. A. Fernandes ◽  
Mário J A Saad ◽  
Lício A Velloso


Diabetes ◽  
2005 ◽  
Vol 54 (5) ◽  
pp. 1447-1451 ◽  
Author(s):  
S. J. Fisher ◽  
J. C. Bruning ◽  
S. Lannon ◽  
C. R. Kahn


1991 ◽  
Vol 260 (5) ◽  
pp. R854-R861 ◽  
Author(s):  
L. J. Guillette ◽  
D. H. Dubois ◽  
A. Cree

Extensive data show that in mammals and birds, prostaglandins (PGs) are associated with ovulation, luteal function, oviposition, and parturition, and that also in mammals they are associated with birth-related behavior and sexual receptivity. In mammals and birds, the ability of PGs to stimulate oviducal contractions varies regionally along the oviduct (i.e., there is a functional cervix or uterovaginal region that acts to retain eggs or embryos in utero during shelling or embryonic development). Furthermore, at least in mammals, there is neural control over oviducal contractions. In reptiles, PGs stimulate oviducal contractions, and these contractions may be overridden by neural control. No data are available on whether PGs stimulate oviducal contractions in amphibians or whether there is a functional cervix in amphibians or reptiles. We suggest that in ancestral amphibians with oviparity and external fertilization, eggs moved rapidly through the oviduct after ovulation and that ovarian and oviducal PGF served as an endocrine hormone coordinating oviducal contractions and central nervous system-controlled oviposition behavior. Furthermore, we hypothesize that there was little or no neural control over oviducal contractions and no functional cervix. These conditions may still exist in present-day oviparous amphibians. In contrast, we suggest that modern-day oviparous reptiles have evolved a functional cervix and neural control over PG-induced uterine contractions, allowing egg passage to be blocked and thus the development of egg retention. These characteristics may be viewed as exaptations for the evolution of viviparity.



2015 ◽  
Vol 29 (9) ◽  
pp. 1303-1319 ◽  
Author(s):  
Michael J. Williams ◽  
Anders Eriksson ◽  
Muksheed Shaik ◽  
Sarah Voisin ◽  
Olga Yamskova ◽  
...  

Abstract Several genome-wide association studies have linked the Nudix hydrolase family member nucleoside diphosphate-linked moiety X motif 3 (NUDT3) to obesity. However, the manner of NUDT3 involvement in obesity is unknown, and NUDT3 expression, regulation, and signaling in the central nervous system has not been studied. We performed an extensive expression analysis in mice, as well as knocked down the Drosophila NUDT3 homolog Aps in the nervous system, to determine its effect on metabolism. Detailed in situ hybridization studies in the mouse brain revealed abundant Nudt3 mRNA and protein expression throughout the brain, including reward- and feeding-related regions of the hypothalamus and amygdala, whereas Nudt3 mRNA expression was significantly up-regulated in the hypothalamus and brainstem of food-deprived mice. Knocking down Aps in the Drosophila central nervous system, or a subset of median neurosecretory cells, known as the insulin-producing cells (IPCs), induces hyperinsulinemia-like phenotypes, including a decrease in circulating trehalose levels as well as significantly decreasing all carbohydrate levels under starvation conditions. Moreover, lowering Aps IPC expression leads to a decreased ability to recruit these lipids during starvation. Also, loss of neuronal Aps expression caused a starvation susceptibility phenotype while inducing hyperphagia. Finally, the loss of IPC Aps lowered the expression of Akh, Ilp6, and Ilp3, genes known to be inhibited by insulin signaling. These results point toward a role for this gene in the regulation of insulin signaling, which could explain the robust association with obesity in humans.





2008 ◽  
Vol 109 (1) ◽  
pp. 137-148 ◽  
Author(s):  
J A. Jeevendra Martyn ◽  
Masao Kaneki ◽  
Shingo Yasuhara ◽  
David S. Warner ◽  
Mark A. Warner

Obesity is a major cause of type 2 diabetes, clinically evidenced as hyperglycemia. The altered glucose homeostasis is caused by faulty signal transduction via the insulin signaling proteins, which results in decreased glucose uptake by the muscle, altered lipogenesis, and increased glucose output by the liver. The etiology of this derangement in insulin signaling is related to a chronic inflammatory state, leading to the induction of inducible nitric oxide synthase and release of high levels of nitric oxide and reactive nitrogen species, which together cause posttranslational modifications in the signaling proteins. There are substantial differences in the molecular mechanisms of insulin resistance in muscle versus liver. Hormones and cytokines from adipocytes can enhance or inhibit both glycemic sensing and insulin signaling. The role of the central nervous system in glucose homeostasis also has been established. Multipronged therapies aimed at rectifying obesity-induced anomalies in both central nervous system and peripheral tissues may prove to be beneficial.





2006 ◽  
Vol 79 (4) ◽  
pp. 205-221 ◽  
Author(s):  
Lars P. van der Heide ◽  
Geert M.J. Ramakers ◽  
Marten P. Smidt


Diabetes ◽  
2015 ◽  
Vol 64 (10) ◽  
pp. 3413-3424 ◽  
Author(s):  
Pei-Wen Cheng ◽  
Ying-Ying Chen ◽  
Wen-Han Cheng ◽  
Pei-Jung Lu ◽  
Hsin-Hung Chen ◽  
...  


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