Hoodia gordonii extract targets both adipose and muscle tissue to achieve weight loss in rats

2014 ◽  
Vol 155 (2) ◽  
pp. 1284-1290 ◽  
Author(s):  
Carine Smith ◽  
Annadie Krygsman
2018 ◽  
Vol 43 (2) ◽  
pp. 187-193 ◽  
Author(s):  
Dongmei Liu ◽  
Flor Elisa Morales ◽  
Heidi. B. IglayReger ◽  
Mary K. Treutelaar ◽  
Amy E. Rothberg ◽  
...  

Local inflammation in obese adipose tissue has been shown to contribute to insulin resistance; however, the role of macrophage infiltration within skeletal muscle is still debatable. This study aimed to evaluate the association of skeletal muscle macrophage gene expression with adiposity levels and insulin sensitivity in obese patients. Twenty-two nondiabetic obese patients and 23 healthy lean controls were included. Obese patients underwent a 3-month weight loss intervention. Macrophage gene expression in skeletal muscle (quantitative real-time polymerase chain reaction), body composition (dual-energy X-ray absorptiometry), and insulin sensitivity (homeostatic model assessment (HOMA) and oral glucose tolerance test) were compared between groups and their associations were analyzed. To validate skeletal muscle findings, we repeated the analyses with macrophage gene expression in adipose tissue. Expression levels of macrophage genes (CD68, CD11b, CD206, CD16, CD40, and CD163) were lower in skeletal muscle tissue of obese versus lean participants. Macrophage gene expression was also found to be inversely associated with adiposity, fasting insulin, and HOMA (r = −0.4 ∼ −0.6, p < 0.05), as well as positively associated with insulin sensitivity (r = 0.4 ∼ 0.8, p < 0.05). On the other hand, adipose tissue macrophage gene expression showed higher levels in obese versus lean participants, presenting a positive association with adiposity levels. Macrophage gene expression, in both skeletal and adipose tissue samples, was only minimally affected by the weight loss intervention. In contrast with the established positive relationship between adiposity and macrophage gene expression, an unexpected inverse correlation between these 2 variables was observed in skeletal muscle tissue. Additionally, muscle macrophage gene expression was inversely correlated with insulin resistance.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Josep M. Argilés ◽  
Britta Stemmler ◽  
Francisco J. López-Soriano ◽  
Silvia Busquets

Cachexia is a syndrome associated with cancer, characterized by body weight loss, muscle and adipose tissue wasting, and inflammation, being often associated with anorexia. In spite of the fact that muscle tissue represents more than 40% of body weight and seems to be the main tissue involved in the wasting that occurs during cachexia, recent developments suggest that tissues/organs such as adipose (both brown and white), brain, liver, gut, and heart are directly involved in the cachectic process and may be responsible for muscle wasting. This suggests that cachexia is indeed a multiorgan syndrome. Bearing all this in mind, the aim of the present review is to examine the impact of nonmuscle tissues in cancer cachexia.


1964 ◽  
Vol 45 (1) ◽  
pp. 68-78 ◽  
Author(s):  
Georgina Faludi ◽  
Lewis C. Mills ◽  
Zev W. Chayes

ABSTRACT Myopathy was induced in dogs with large doses of anti-inflammatory steroids (cortisol, prednisolone, methylprednisolone, dexamethasone and triamcinolone). Weight loss and muscle atrophy occurred in all groups except the control group but was most pronounced in the triamcinolone-treated dogs. There was a marked difference between the treated groups in decrease of muscle size (occurring the least with cortisol) and also in fiber thickness of muscle tissue (changing the least methylprednisolone and diminishing the most triamcinolone). The diagnosis of steroid myopathy could be made by clinical observation, electromyography and biopsy. The only specific histological change detectable was the diminished size of muscle fiber. Further investigation is necessary to understand the pathogenesis and to explain the peculiar localization of the myopathy.


Ob Gyn News ◽  
2008 ◽  
Vol 43 (4) ◽  
pp. 20
Author(s):  
MICHELE G. SULLIVAN

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