scholarly journals Epididymal Fat Is Necessary for Spermatogenesis, but not Testosterone Production or Copulatory Behavior

Endocrinology ◽  
2010 ◽  
Vol 151 (12) ◽  
pp. 5669-5679 ◽  
Author(s):  
Ye Chu ◽  
Gloria G. Huddleston ◽  
Andrew N. Clancy ◽  
Ruth B. S. Harris ◽  
Timothy J. Bartness
Keyword(s):  
Adipose Tissue ◽  
Sertoli Cells ◽  
Marked Decrease ◽  
Copulatory Behavior ◽  
Surgical Removal ◽  
Laboratory Rats ◽  
Sham Surgery ◽  
Serum Lh ◽  
Epididymal White Adipose Tissue ◽  
Testicular Histology

Surgical removal of the epididymal white adipose tissue (EWAT) depot (lipectomy; EWATx) in laboratory rats or mice decreases spermatogenesis, but this phenomenal finding has not been investigated in depth. Specifically, detailed histology, neuroendocrine profiles, copulatory behavior, lipectomy of other WAT depots, rescue by autologous EWAT transplants, or tests whether this EWATx effect is due to disruption of testes innervation occurring during EWATx have not been performed. Therefore, in the first study, we performed EWATx in male Syrian hamsters and attempted to rescue spermatogenesis by transplanting the removed EWAT to the animal’s subcutaneous dorsum, removed comparable or larger amounts of non-gonadal WAT [inguinal WAT (IWAT)] and conducted mating behavior tests. In a second study we conducted detailed testicular histology and assayed serum LH, FSH, and testosterone (T). In a third study, we surgically denervated the testes without removing EWAT and compared testicular histology with that of EWATx or sham surgery. We found that EWATx, but not IWATx, virtually eliminated spermatogenesis producing a marked decrease in size of the seminiferous tubule cellular lining including the Sertoli cells and spermatogonia that could not be rescued by autologous EWAT transplant to the subcutaneous dorsum. EWATx did not change serum LH or T concentrations but approximately doubled serum FSH concentrations. EWATx did not alter copulatory behavior but resulted in aspermatic ejaculate. Selective surgical testicular denervation did not affect spermatogenesis. Collectively, these results suggest the presence of a local, but currently unidentified, growth and/or nutritive factor from EWAT that promotes spermatogenesis.

scholarly journals Decrease of Obesity by Allantoin via Imidazoline I1-Receptor Activation in High Fat Diet-Fed Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Hsien-Hui Chung ◽  
Kung Shing Lee ◽  
Juei-Tang Cheng
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Intake ◽  
High Fat Diet ◽  
Chronic Administration ◽  
Receptor Activation ◽  
Inhibitory Effect ◽  
High Fat ◽  
Epididymal White Adipose Tissue ◽  
The Brain

The activation of the imidazoline I1-receptor (I1R) is known to regulate appetite. Allantoin, an active ingredient in the yam, has been reported to improve lipid metabolism in high fat diet- (HFD-)fed mice. However, the effect of allantoin on obesity remains unclear. In the present study, we investigated the effects of allantoin on HFD-induced obesity. The chronic administration of allantoin to HFD-fed mice for 8 weeks significantly decreased their body weight, and this effect was reversed by efaroxan at a dose sufficient to block I1R. The epididymal white adipose tissue (eWAT) cell size and weight in HFD-fed mice were also decreased by allantoin via the activation of I1R. In addition, allantoin significantly decreased the energy intake of HFD-fed mice, and this reduction was associated with a decrease in the NPY levels in the brain. However, no inhibitory effect of allantoin on energy intake was observed in db/db mice. Moreover, allantoin lowered HFD-induced hyperleptinemia, and this activity was abolished by I1R blockade with efaroxan. Taken together, these data suggest that allantoin can ameliorate energy intake and eWAT accumulation by activating I1R to improve HFD-induced obesity.

Detection of 2-Alkylcyclobutanones, Markers for Irradiated Foods, in Adipose Tissues of Animals Fed with These Substances

2002 ◽  
Vol 65 (10) ◽  
pp. 1610-1613 ◽  
Author(s):  
P. HORVATOVICH ◽  
F. RAUL ◽  
M. MIESCH ◽  
D. BURNOUF ◽  
H. DELINCEE ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Intestinal Barrier ◽  
Adipose Tissues ◽  
Laboratory Rats ◽  
Irradiated Foods ◽  
Drinking Fluid

Laboratory rats received a freshly prepared drinking fluid containing 0.005% 2-tetradecyl- or 2-tetradecenyl-cyclobutanones daily for 4 months. These two compounds were recovered in the adipose tissues of the animals that consumed them. Less than 1% of the 2-alkylcyclobutanones ingested daily were excreted in the feces. In addition, our data indicate that 2-alkylcyclobutanones are able to cross the intestinal barrier, to enter into the bloodstream, and to be stored in the adipose tissue of an animal. However, the amounts of these substances detected in the adipose tissues and in the feces were much smaller than the amounts ingested.

scholarly journals Effects of Ca2+ and Mg2+ on the activity of pyruvate dehydrogenase phosphate phosphatase within toluene-permeabilized mitochondria

1987 ◽  
Vol 241 (2) ◽  
pp. 371-377 ◽  
Author(s):  
P J Midgley ◽  
G A Rutter ◽  
A P Thomas ◽  
R M Denton
Keyword(s):  
Adipose Tissue ◽  
Small Molecules ◽  
White Adipose Tissue ◽  
Pyruvate Dehydrogenase ◽  
Maximum Rate ◽  
Major Effect ◽  
Lag Phase ◽  
Inhibitory Effects ◽  
Highly Sensitive ◽  
Epididymal White Adipose Tissue

Mitochondria from rat epididymal white adipose tissue were made permeable to small molecules by toluene treatment and were used to investigate the effects of Mg2+ and Ca2+ on the re-activation of pyruvate dehydrogenase phosphate by endogenous phosphatase. Re-activation of fully phosphorylated enzyme after addition of 0.18 mM-Mg2+ showed a marked lag of 5-10 min before a maximum rate of reactivation was achieved. Increasing the Mg2+ concentration to 1.8 mM (near saturating) or the addition of 100 microM-Ca2+ resulted in loss of the lag phase, which was also greatly diminished if pyruvate dehydrogenase was not fully phosphorylated. It is concluded that, within intact mitochondria, phosphatase activity is highly sensitive to the degree of phosphorylation of pyruvate dehydrogenase and that the major effect of Ca2+ may be to overcome the inhibitory effects of sites 2 and 3 on the dephosphorylation of site 1. Apparent K0.5 values for Mg2+ and Ca2+ were determined from the increases in pyruvate dehydrogenase activity observed after 5 min. The K0.5 for Mg2+ was diminished from 0.60 mM at less than 1 nM-Ca2+ to 0.32 mM at 100 microM-Ca2+; at 0.18 mM-Mg2+, the K0.5 for Ca2+ was 0.40 microM. Ca2+ had little or no effect at saturating Mg2+ concentrations. Since effects of Ca2+ are readily observed in intact coupled mitochondria, it follows that Mg2+ concentrations within mitochondria are sub-saturating for pyruvate dehydrogenase phosphate phosphatase and hence less than 0.5 mM.

scholarly journals Role of insulin receptors in the changing metabolism of adipose tissue during pregnancy and lactation in the rat

1979 ◽  
Vol 182 (2) ◽  
pp. 421-427 ◽  
Author(s):  
D J Flint ◽  
P A Sinnett-Smith ◽  
R A Clegg ◽  
R G Vernon
Keyword(s):  
Adipose Tissue ◽  
Marked Decrease ◽  
Normal Values ◽  
Serum Insulin ◽  
Insulin Receptors ◽  
Acid Synthesis ◽  
Anabolic Activity ◽  
Pregnancy And Lactation ◽  
Metabolic Activities

Changes in the volume, the rates of fatty acid synthesis and synthesis of the glycerol moiety of acylglycerols, the activity of lipoprotein lipase, and the number and affinity of insulin receptors of adipocytes, and concentrations of serum insulin, prolactin and progesterone were determined in virgin rats and in rats at various stages of pregnancy and lactation. Changes in the metabolic activities of adipose tissue appeared to be synchronized and primarily comprised a marked decrease in anabolic activity around parturition. In contrast, the number of insulin receptors (Kd 1.5 nM) per adipocyte doubled during pregnancy before returning to normal values around parturition. It is postulated that the increase in the number of insulin receptors is an adaptation to counteract the effects of insulin-antagonistic hormones during pregnancy and that the decrease in the number of receptors is primarily responsible for the loss of anabolic activity around parturition.

scholarly journals Metformin induces oxidative stress in white adipocytes and raises uncoupling protein 2 levels

2008 ◽  
Vol 199 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Andrea Anedda ◽  
Eduardo Rial ◽  
M Mar González-Barroso
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Protein Levels ◽  
White Adipocytes ◽  
Epididymal White Adipose Tissue ◽  
Amp Activated Protein Kinase

Metformin is a drug widely used to treat type 2 diabetes. It enhances insulin sensitivity by improving glucose utilization in tissues like liver or muscle. Metformin inhibits respiration, and the decrease in cellular energy activates the AMP-activated protein kinase that in turn switches on catabolic pathways. Moreover, metformin increases lipolysis and β-oxidation in white adipose tissue, thereby reducing the triglyceride stores. The uncoupling proteins (UCPs) are transporters that lower the efficiency of mitochondrial oxidative phosphorylation. UCP2 is thought to protect against oxidative stress although, alternatively, it could play an energy dissipation role. The aim of this work was to analyse the involvement of UCP2 on the effects of metformin in white adipocytes. We studied the effect of this drug in differentiating 3T3-L1 adipocytes and found that metformin causes oxidative stress since it increases the levels of reactive oxygen species (ROS) and lowers the aconitase activity. Variations in UCP2 protein levels parallel those of ROS. Metformin also increases lipolysis in these cells although only when the levels of ROS and UCP2 have decreased. Hence, UCP2 does not appear to be needed to facilitate fatty acid oxidation. Furthermore, treatment of C57BL/6 mice with metformin also augmented the levels of UCP2 in epididymal white adipose tissue. We conclude that metformin treatment leads to the overexpression of UCP2 in adipocytes to minimize the oxidative stress that is probably due to the inhibition of respiration caused by the drug.

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