An activated sympathetic nervous system affects white adipocyte differentiation and lipolysis in a rat model of Parkinson's disease

2014 ◽  
Vol 93 (2) ◽  
pp. 350-360 ◽  
Author(s):  
XiangZhi Meng ◽  
RuiPan Zheng ◽  
Ying Zhang ◽  
MingLiang Qiao ◽  
Li Liu ◽  
...  
1997 ◽  
Vol 148 (1) ◽  
pp. 135-146 ◽  
Author(s):  
Clive N. Svendsen ◽  
Maeve A. Caldwell ◽  
Jinkun Shen ◽  
Melanie G. ter Borg ◽  
Anne E. Rosser ◽  
...  

2015 ◽  
Vol 28 (3) ◽  
pp. 423-431 ◽  
Author(s):  
D. W. Gil ◽  
J. Wang ◽  
C. Gu ◽  
J. E. Donello ◽  
S. Cabrera ◽  
...  

2002 ◽  
Vol 227 (6) ◽  
pp. 363-376 ◽  
Author(s):  
Timothy J. Bartness ◽  
Gregory E. Demas ◽  
C. Kay Song

It appears advantageous for many non-human animals to store energy body fat extensively and efficiently because their food supply is more labile and less abundant than in their human counterparts. The level of adiposity in many of these species often shows predictable increases and decreases with changes in the season. These cyclic changes in seasonal adiposity in some species are triggered by changes in the photoperiod that are faithfully transduced into a biochemical signal through the nightly secretion of melatonin (MEL) via the pineal gland. Here, we focus primarily on the findings from the most commonly studied species showing seasonal changes in adiposity—Siberian and Syrian hamsters. The data to date are not compelling for a direct effect of MEL on white adipose tissue (WAT) and brown adipose tissue (BAT) despite some recent data to the contrary. Thus far, none of the possible hormonal intermediaries for the effects of MEL on seasonal adiposity appear likely as a mechanism by which MEL affects the photoperiodic control of body fat levels indirectly. We also provide evidence pointing toward the sympathetic nervous system as a likely mediator of the effects of MEL on short day-induced body fat decreases in Siberian hamsters through increases in sympathetic drive on WAT and BAT. We speculate that decreases in the SNS drive to these tissues may underlie the photoperiod-induced seasonal increases in body fat of species such as Syrian hamsters. Clearly, we need to deepen our understanding of seasonal adiposity, although, to our knowledge, this is the only form of environmentally induced changes in body fat where the key elements of its external trigger have been identified and can be traced to and through their transduction into a physiological stimulus that ultimately affects identified responses of white adipocyte physiology and cellularity. Finally, the comparative physiological approach to the study of seasonal adiposity seems likely to continue to yield significant insights into the mechanisms underlying this phenomenon and for understanding obesity and its reversal in general.


2021 ◽  
Vol 21 (2) ◽  
pp. 1176-1183
Author(s):  
Li Xu ◽  
Tuexun Mayila ◽  
Jie Wang

Parkinson’s disease is a degenerative disease of the central nervous system, and it occurs in middle-aged and elderly people. Studies have shown that both the clinical symptoms and neuropathological evidence of Parkinson’s disease suggest that Parkinson’s disease may originate in the gut. Intestinal flora homeostasis plays an important role in maintaining normal functions of the brain and nervous system. It participates in changes in cellular flora through oxidative stress, inflammatory response, and immune response during metabolism. Intestinal flora disorders are closely related to the onset of neurological diseases such as Parkinson’s disease (PD). In order to better understand the relationship between intestinal flora and Parkinson’s disease, this article studies the correlation between PD rat models and intestinal flora, and analyzes the possible relationship between them. The 6-OHDA PD rat model is currently a better model preparation method, which is widely used in PD research. The experimental results show that using Fe3O4 nanoparticle technology to detect intestinal flora disorders in PD patients, and the role of intestinal flora disorders in Parkinson’s disease may include affecting inflammatory response and oxidative stress, α-synuclein Protein (α-syn), these modes of action are not independent, there are complex and synergistic effects, and the molecular simulation mechanism may play a key role in these effects. There is a certain relationship between intestinal flora and Parkinson’s disease, but the specific mechanism is not clear, and further research is needed to provide more directions for the early diagnosis and early treatment of PD.


Neuroscience ◽  
1995 ◽  
Vol 67 (4) ◽  
pp. 941-951 ◽  
Author(s):  
J.A. Desmeules ◽  
V. Kayser ◽  
J. Weil-Fuggaza ◽  
A. Bertrand ◽  
G. Guilbaud

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S392-S392
Author(s):  
Nadja Van Camp ◽  
Koen Van Laere ◽  
Ruth Vreys ◽  
Marleen Verhoye ◽  
Erwin Lauwers ◽  
...  

1981 ◽  
Vol 97 (1) ◽  
pp. 91-97 ◽  
Author(s):  
H. Storm ◽  
C. van Hardeveld ◽  
A. A. H. Kassenaar

Abstract. Basal plasma levels for adrenalin (A), noradrenalin (NA), l-triiodothyronine (T3), and l-thyroxine (T4) were determined in rats with a chronically inserted catheter. The experiments described in this report were started 3 days after the surgical procedure when T3 and T4 levels had returned to normal. Basal levels for the catecholamines were reached already 4 h after the operation. The T3/T4 ratio in plasma was significantly increased after 3, 7, and 14 days in rats kept at 4°C and the same holds for the iodide in the 24-h urine after 7 and 14 days at 4°C. The venous NA plasma concentration was increased 6- to 12-fold during the same period of exposure to cold, whereas the A concentration remained at the basal level. During infusion of NA at 23°C the T3/T4 ratio in plasma was significantly increased after 7 days compared to pair-fed controls, and the same holds for the iodide excretion in the 24-h urine. This paper presents further evidence for a role of the sympathetic nervous system on T4 metabolism in rats at resting conditions.


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