scholarly journals Inhibition of Cisplatin-Induced Lipid Catabolism and Weight Loss by Ghrelin in Male Mice

Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3118-3129 ◽  
Author(s):  
Jose M. Garcia ◽  
Thomas Scherer ◽  
Ji-an Chen ◽  
Bobby Guillory ◽  
Anriada Nassif ◽  
...  

Cachexia, defined as an involuntary weight loss ≥5%, is a serious and dose-limiting side effect of chemotherapy that decreases survival in cancer patients. Alterations in lipid metabolism are thought to cause the lipodystrophy commonly associated with cachexia. Ghrelin has been proposed to ameliorate the alterations in lipid metabolism due to its orexigenic and anabolic properties. However, the mechanisms of action through which ghrelin could potentially ameliorate chemotherapy-associated cachexia have not been elucidated. The objectives of this study were to identify mechanisms by which the chemotherapeutic agent cisplatin alters lipid metabolism and to establish the role of ghrelin in reversing cachexia. Cisplatin-induced weight and fat loss were prevented by ghrelin. Cisplatin increased markers of lipolysis in white adipose tissue (WAT) and of β-oxidation in liver and WAT and suppressed lipogenesis in liver, WAT, and muscle. Ghrelin prevented the imbalance between lipolysis, β-oxidation, and lipogenesis in WAT and muscle. Pair-feeding experiments demonstrated that the effects of cisplatin and ghrelin on lipogenesis, but not on lipolysis and β-oxidation, were due to a reduction in food intake. Thus, ghrelin prevents cisplatin-induced weight and fat loss by restoring adipose tissue functionality. An increase in caloric intake further enhances the anabolic effects of ghrelin.

2010 ◽  
Vol 7 (4) ◽  
pp. 8-11 ◽  
Author(s):  
N A Petunina ◽  
N E Al'tshuler ◽  
N G Rakova ◽  
L V Trukhina

The review presents a recent data from the literature on the physiologic and pathophysiologic role of adipose tissue hormones (adiponectin, resistin, leptin). The article details the role of adipocytokines in atherogenesis. It also presents the results of studies depicting the relationship between subclinical hypothyroidism, lipid metabolism and insulin resistance as well as the impact of thyroid dysfunction upon the secretion of adipocytokines.


2016 ◽  
Vol 15 (1) ◽  
Author(s):  
Xiaoliang Shao ◽  
Wei Yang ◽  
Xiaonan Shao ◽  
Chun Qiu ◽  
Xiaosong Wang ◽  
...  

2009 ◽  
Vol 296 (5) ◽  
pp. E1120-E1132 ◽  
Author(s):  
Christelle Veyrat-Durebex ◽  
Xavier Montet ◽  
Manlio Vinciguerra ◽  
Asllan Gjinovci ◽  
Paolo Meda ◽  
...  

The inbred Lou/C rat, originating from the Wistar strain, has been described as a model of resistance to diet-induced obesity, but little is known about its metabolism. Since this knowledge could provide some clues about the etiology of obesity/insulin resistance, this study aimed at characterizing glucose and lipid metabolism in Lou/C vs. Wistar rats. This was achieved by performing glucose and insulin tolerance tests, euglycemic hyperinsulinemic clamps, and characterization of intracellular insulin signaling in skeletal muscle. Substrate-induced insulin secretion was evaluated using perfused pancreas and isolated islets. Finally, body fat composition and the expression of various factors involved in lipid metabolism were determined. Body weight and caloric intake were lower in Lou/C than in Wistar rats, whereas food efficiency was similar. Improved glucose tolerance of Lou/C rats was not related to increased insulin output but was related to improved insulin sensitivity/responsiveness in the liver and in skeletal muscles. In the latter tissue, this was accompanied by improved insulin signaling, as suggested by higher activation of the insulin receptor and of the Akt/protein kinase B pathway. Fat deposition was markedly lower in Lou/C than in Wistar rats, especially in visceral adipose tissue. In the inguinal adipose depot, expression of uncoupling protein-1 was detected in Lou/C but not in Wistar rats, in keeping with a higher expression of peroxisome proliferator-activated receptor-γ coactivator-1 in these animals. The Lou/C rat is a valuable model of spontaneous food restriction with associated improved insulin sensitivity. Independently from its reduced caloric intake, it also exhibits a preferential channeling of nutrients toward utilization rather than storage.


1984 ◽  
Vol 8 (2) ◽  
pp. 147-159 ◽  
Author(s):  
R.E. Catalán ◽  
A.M. Martínez ◽  
M.D. Aragonés

2021 ◽  
Author(s):  
Raghbendra Kumar Dutta ◽  
Joon No Lee ◽  
Yunash Maharjan ◽  
Channy Park ◽  
Seong-Kyu Choe ◽  
...  

Abstract Background Fatty acids (FA) derived from adipose tissue and liver serve as the main fuel in thermogenesis of brown adipose tissue (BAT). Catalase, a peroxisomal enzyme, plays an important role in maintaining intracellular redox homeostasis by decomposing hydrogen peroxide to either water or oxygen that oxidize and provide fuel for cellular metabolism. Although the antioxidant enzymatic activity of catalase is well known, its role in the metabolism and maintenance of energy homeostasis has not yet been revealed. The present study investigated the role of catalase in lipid metabolism and thermogenesis during nutrient deprivation in catalase-knockout (KO) mice. Results We found that hepatic triglyceride accumulation in KO mice decreased during sustained fasting due to lipolysis through reactive oxygen species (ROS) generation in adipocytes. Furthermore, the free FA released from lipolysis were shuttled to BAT through the activation of CD36 and catabolized by lipoprotein lipase in KO mice during sustained fasting. Although the exact mechanism for the activation of the FA receptor enzyme is still unclear, we found that ROS generation in adipocytes mediated the shuttling of FA to BAT. Conclusions Taken together, our findings uncover the novel role of catalase in lipid metabolism and thermogenesis in BAT, which may be useful in understanding metabolic dysfunction.


2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Maria Chondronikola ◽  
Craig Porter ◽  
Nicholas Hurren ◽  
Tony Chao ◽  
Christina Yfanti ◽  
...  

2018 ◽  
Vol 20 (5) ◽  
pp. 1280-1288 ◽  
Author(s):  
Prince Dadson ◽  
Jarna C. Hannukainen ◽  
Mueez U Din ◽  
Minna Lahesmaa ◽  
Kari K. Kalliokoski ◽  
...  

2018 ◽  
Vol 6 (13) ◽  
pp. e13735 ◽  
Author(s):  
Birgitta W. van der Kolk ◽  
Roel G. Vink ◽  
Johan W. E. Jocken ◽  
Nadia J. T. Roumans ◽  
Gijs H. Goossens ◽  
...  

Author(s):  
Zhengtang Qi ◽  
Shuzhe Ding

AbstractObesity in children and adolescents is characterized by chronic sympathetic overdrive and reduced epinephrine-stimulated lipolysis. This resistance to catecholamines occurs during the dynamic phase of fat accumulation. This review will focus on the relationship between sympathetic-adrenal activity and lipid metabolism, thereby highlighting the role of catecholamine resistance in the development of childhood obesity.Catecholamine resistance causes lipid accumulation in adipose tissue by reducing lipolysis, increasing lipogenesis and impeding free fatty acid (FFA) transportation. Exercise improves catecholamine resistance, as evidenced by attenuated systemic sympathetic activity, reduced circulating catecholamine levels and enhanced β-adrenergic receptor signaling. Insulin resistance is mostly a casual result rather than a cause of childhood obesity. Therefore, catecholamine resistance in childhood obesity may promote insulin signaling in adipose tissue, thereby increasing lipogenesis. This review outlines a series of evidence for the role of catecholamine resistance as an upstream mechanism leading to childhood obesity.


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