scholarly journals Leptin Deficiency and Its Effects on Tibial and Vertebral Bone Mechanical Properties in Mature Genetically Lean and Obese JCR:LA-Corpulent Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Raylene A. Reimer ◽  
Jeremy M. LaMothe ◽  
Ronald F. Zernicke
Keyword(s):  
Mechanical Properties ◽  
Leptin Receptor ◽  
Lumbar Vertebrae ◽  
Insulin Resistance Syndrome ◽  
Proportional Limit ◽  
Leptin Signaling ◽  
Bone Mechanical Properties ◽  
Geometrical Properties ◽  
Leptin Deficiency ◽  
Obese Rats

Leptin signaling deficient rodents have emerged as models of obesity/insulin resistance syndrome. Altered leptin signaling, however, can affect axial and appendicular bone geometrical properties differently, and, thus, we hypothesized that leptin-deficiency would differentially influence mechanical properties of vertebrae and tibiae compared to lean rats. Mature (9 mo) leptin receptor deficient obese (cp/cp;n=8) and lean (+/?;n=7) male JCR:LA-corpulent rats were used to test that hypothesis. Tibiae and the sixth lumbar vertebrae(L6)were scanned with micro-CT and were broken in three point-bending (tibiae) or axial loading(L6). Supporting the hypothesis, vertebrae and tibiae were differentially affected by leptin signaling deficiency. Tibiae, but not vertebrae, were significantly shorter in obese rats and achieved a significantly greater load (>18%), displacement (>15%), and stress (>18%) at the proportional limit, relative to the lean rats. Conversely,L6in obese rats had significantly reduced displacement (>25%) and strain (>32%) at proportional limit, relative to the lean rats. Those combined results suggest that the etiology and duration of obesity may be important determinants of bone mechanical properties, and axial and appendicular bones may be affected differently.

Upregulation of the leptin receptor as a mechanism to overcome leptin deficiency in apoptotic processes and miscarriages

2014 ◽  
Vol 101-102 ◽  
pp. 54
Author(s):  
Aurelia Pestka ◽  
B. Toth ◽  
C. Kuhn ◽  
I. Wiest ◽  
C. Hoffmann ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Leptin Deficiency

Analysis of Mechanophysical Properties of Fritillaria ussuriensis Maxim and Designing of Grade Sieve Machine

2013 ◽  
Vol 764 ◽  
pp. 165-168
Author(s):  
Jiang Song ◽  
Song Zhuo Lu ◽  
Li Hua Liu ◽  
Ming Wang ◽  
Tian Xiang Liu
Keyword(s):  
Mechanical Properties ◽  
Friction Coefficient ◽  
Physical And Mechanical Properties ◽  
Middle Layer ◽  
Mathematical Statistics ◽  
Angle Of Repose ◽  
Screening Process ◽  
Geometrical Properties ◽  
Pore Dimension ◽  
Main Index

Based on the field and lab measuerement in harvest time, Physical and mechanical properties of fritillaria ussuriensis maxim (FUM) are researched. Geometrical properties of FUM are analyzed using mathematical statistics method, and the variation sections of main index values of two kinds of FUM are obtained. Mechanical properties of FUM outsifting in screen penetrating process are tested by means of friction experiment, the friction coefficient and angle of repose of two kinds of FUM are obtained using mathematical statistics method. Grade sieve machine is designed based on the analysis of mechanophysical properties of FUM. The main parameters are: shape of sieve pore is rectangle, screen diameter is 20mm, sieve pore dimension of upper layer is 13×20mm2, middle layer is 9×18mm2, and under layer is 7×10mm2. By testing of friction coefficient and angle of repose and movement and dynamics analysis of grade sieve, outsifting velocity is 7<<9rad/s and acceleration is 4<a<13m/s2 in screening process.

scholarly journals Endospanin 1 Determines the Balance of Leptin-Regulated Hypothalamic Functions

2018 ◽  
Vol 108 (2) ◽  
pp. 132-141
Author(s):  
Clara Roujeau ◽  
Ralf Jockers ◽  
Julie Dam
Keyword(s):  
Signaling Pathways ◽  
Intracellular Trafficking ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Human Obesity ◽  
Leptin Signaling ◽  
Diet Induced Obesity ◽  
Important Regulator ◽  
Neuronal Plasma Membrane ◽  
Underlying Mechanisms

Endospanin 1 (Endo1), a protein encoded in humans by the same gene than the leptin receptor (ObR), and increased by diet-induced obesity, is an important regulator of ObR trafficking and cell surface exposure, determining leptin signaling strength. Defective intracellular trafficking of the leptin receptor to the neuronal plasma membrane has been proposed as a mechanism underlying the development of leptin resistance observed in human obesity. More recently, Endo1 has emerged as a mediator of “selective leptin resistance.” The underlying mechanisms of the latter are not completely understood, but the possibility of differential activation of leptin signaling pathways was suggested among others. In this respect, the expression level of Endo1 is crucial for the appropriate balance between different leptin signaling pathways and leptin functions in the hypothalamus and is likely participating in selective leptin resistance for the control of energy and glucose homeostasis.

scholarly journals Leptin receptor expression in the dorsomedial hypothalamus stimulates breathing during NREM sleep in db/db mice

SLEEP ◽  
2021 ◽  
Author(s):  
Huy Pho ◽  
Slava Berger ◽  
Carla Freire ◽  
Lenise J Kim ◽  
Mi-Kyung Shin ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Leptin Receptor ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Upper Airway Obstruction ◽  
Co2 Production ◽  
Dorsomedial Hypothalamus ◽  
Leptin Signaling ◽  
Arterial Blood ◽  
Obesity Hypoventilation

Abstract Study Objectives Obesity leads to obstructive sleep apnea (OSA), which is recurrent upper airway obstruction during sleep, and obesity hypoventilation syndrome (OHS), hypoventilation during sleep resulting in daytime hypercapnia. Impaired leptin signaling in the brain was implicated in both conditions, but mechanisms are unknown. We have previously shown that leptin stimulates breathing and treats OSA and OHS in leptin- deficient ob/ob mice and leptin-resistant diet-induced obese mice and that leptin’s respiratory effects may occur in the dorsomedial hypothalamus (DMH). We hypothesized that leptin receptor LepR b–deficient db/db mice have obesity hypoventilation and that restoration of leptin signaling in the DMH will increase ventilation during sleep in these animals. Methods We measured arterial blood gas in unanesthetized awake db/db mice. We subsequently infected these animals with Ad-LepR  b or control Ad-mCherry virus into the DMH and measured ventilation during sleep as well as CO2 production after intracerebroventricular (ICV) infusions of phosphate-buffered saline or leptin. Results Awake db/db mice had elevated CO2 levels in the arterial blood. Ad-LepR  b infection resulted in LepR  b expression in the DMH neurons in a similar fashion to wildtype mice. In LepR  b-DMH db/db mice, ICV leptin shortened REM sleep and increased inspiratory flow, tidal volume and minute ventilation during NREM sleep without any effect on the quality of NREM sleep or CO2 production. Leptin had no effect on upper airway obstruction in these animals. Conclusion Leptin stimulates breathing and treats obesity hypoventilation acting on LepR b-positive neurons in the DMH.

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