scholarly journals Testosterone and Corticosterone in the Mesocorticolimbic System of Male Rats: Effects of Gonadectomy and Caloric Restriction

Endocrinology ◽  
2017 ◽  
Vol 159 (1) ◽  
pp. 450-464 ◽  
Author(s):  
Daniel J Tobiansky ◽  
Anastasia M Korol ◽  
Chunqi Ma ◽  
Jordan E Hamden ◽  
Cecilia Jalabert ◽  
...  
2021 ◽  
Vol 91 ◽  
pp. 108598
Author(s):  
Diego Hernández-Saavedra ◽  
Laura Moody ◽  
Xinyu Tang ◽  
Zachary J. Goldberg ◽  
Alex P. Wang ◽  
...  

2018 ◽  
Vol 7 (4) ◽  
pp. 239-245
Author(s):  
Shohei Dobashi ◽  
Chinatsu Aiba ◽  
Daisuke Ando ◽  
Masataka Kiuchi ◽  
Mitsuya Yamakita ◽  
...  

2004 ◽  
Vol 181 (2) ◽  
pp. 297-306 ◽  
Author(s):  
J Wilsey ◽  
PJ Scarpace

The objectives of this study were to determine if reduced long-form leptin receptor (ObRb) expression in diet-induced obese (DIO) animals is associated with deficits in maximal leptin signaling and, secondly, to establish the effects of short-term caloric restriction (CR) on ObRb expression and function. Groups of DIO and life-long chow-fed (CHOW) F344xBN male rats, aged 6 months, were given an i.c.v. injection containing 2 micro g leptin or artificial cerebrospinal fluid (ACSF) vehicle. Leptin induced a >6-fold increase in STAT3 phosphorylation in CHOW rats, but less than 2-fold increase in DIO. Reduced maximal leptin-stimulated STAT3 phosphorylation in DIO rats was coupled with a decline in both ObRb expression and protein. At this point, subgroups of DIO and CHOW animals underwent CR for 30 days and were then tested for acute leptin responsiveness. CR resulted in a 45 and 85% increase respectively in leptin-stimulated STAT3 phosphorylation in CHOW and DIO animals. Similarly, CR increased ObRb expression and protein in both CHOW and DIO animals. To explore the role of leptin in regulating ObRb expression, we reversibly overexpressed leptin in the hypothalamus and found that ObRb mRNA inversely follows central leptin expression. By enhancing both ObRb expression and signaling capacity, CR may enhance leptin responsiveness in leptin-resistant DIO animals.


2016 ◽  
Vol 311 (1) ◽  
pp. E56-E68 ◽  
Author(s):  
Trevor Teich ◽  
Emily C. Dunford ◽  
Deanna P. Porras ◽  
Jacklyn A. Pivovarov ◽  
Jacqueline L. Beaudry ◽  
...  

Severe caloric restriction (CR), in a setting of regular physical exercise, may be a stress that sets the stage for adiposity rebound and insulin resistance when the food restriction and exercise stop. In this study, we examined the effect of mifepristone, a glucocorticoid (GC) receptor antagonist, on limiting adipose tissue mass gain and preserving whole body insulin sensitivity following the cessation of daily running and CR. We calorically restricted male Sprague-Dawley rats and provided access to voluntary running wheels for 3 wk followed by locking of the wheels and reintroduction to ad libitum feeding with or without mifepristone (80 mg·kg−1·day−1) for 1 wk. Cessation of daily running and CR increased HOMA-IR and visceral adipose mass as well as glucose and insulin area under the curve during an oral glucose tolerance test vs. pre-wheel lock exercised rats and sedentary rats (all P < 0.05). Insulin sensitivity and glucose tolerance were preserved and adipose tissue mass gain was attenuated by daily mifepristone treatment during the post-wheel lock period. These findings suggest that following regular exercise and CR there are GC-induced mechanisms that promote adipose tissue mass gain and impaired metabolic control in healthy organisms and that this phenomenon can be inhibited by the GC receptor antagonist mifepristone.


2018 ◽  
Vol 16 (2) ◽  
pp. 49-57
Author(s):  
alireza Delpasand ◽  
Mehrdad Fathi ◽  
Seyyed Reza Attarzadeh Hosseini ◽  
Salma Ahi ◽  
◽  
...  

Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 1208-P
Author(s):  
PALLAVI VARSHNEY ◽  
MICHAEL W. SCHLEH ◽  
CHEEHOON AHN ◽  
AMY ZHENG ◽  
EDWARD B. ARIAS ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. E38-E43 ◽  
Author(s):  
R. Sreekumar ◽  
J. Unnikrishnan ◽  
A. Fu ◽  
J. Nygren ◽  
K. R. Short ◽  
...  

Rodent skeletal muscle mitochondrial DNA has been shown to be a potential site of oxidative damage during aging. Caloric restriction (CR) is reported to reduce oxidative stress and prolong life expectancy in rodents. Gene expression profiling and measurement of mitochondrial ATP production capacity were performed in skeletal muscle of male rats after feeding them either a control diet or calorie-restricted diet (60% of control diet) for 36 wk to determine the potential mechanism of the beneficial effects of CR. CR enhanced the transcripts of genes involved in reactive oxygen free radical scavenging function, tissue development, and energy metabolism while decreasing expression of those genes involved in signal transduction, stress response, and structural and contractile proteins. Real-time PCR measurments confirmed the changes in transcript levels of cytochrome- c oxidase III, superoxide dismutase (SOD)1, and SOD2 that were noted by the microarray approach. Mitochondrial ATP production and citrate synthase were unaltered by the dietary changes. We conclude that CR alters transcript levels of several genes in skeletal muscle and that mitochondrial function in skeletal muscle remains unaltered by the dietary intervention. Alterations in transcripts of many genes involved in reactive oxygen scavenging function may contribute to the increase in longevity reported with CR.


2000 ◽  
Vol 278 (1) ◽  
pp. R231-R237 ◽  
Author(s):  
Barry E. Levin ◽  
Ambrose A. Dunn-Meynell

Half of Sprague-Dawley rats develop and defend diet-induced obesity (DIO) or diet resistance (DR) when fed a high-energy (HE) diet. Here, adult male rats were made DIO or DR after 10 wk on HE diet. Then half of each group was food restricted for 8 wk on chow to maintain their body weights at 90% of their respective baselines. Rate and magnitude of weight loss were comparable, but maintenance energy intake and the degree of sympathetic activity (24-h urine norepinephrine) inhibition were 17 and 29% lower, respectively, in restricted DR than DIO rats. Restricted DIO rats reduced adipose depot weights, plasma leptin, and insulin levels by 35%. Restricted DR rats reduced none of these. When fed ad libitum, both DR and DIO rats returned to the body weights of their respective chow-fed phenotype controls within 2 wk. This was associated with increased adipose mass and leptin and insulin levels only in DIO rats. Thus DR rats appear to alter primarily their lean body mass, whereas DIO rats primarily alter their adipose mass during chronic caloric restriction and refeeding.


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