Chronic increase of circulating galanin levels induces obesity and marked alterations in lipid metabolism similar to metabolic syndrome

Poritsanos, Nicole J.; Mizuno, Tooru M.; Lautatzis, Maria-Elena; Vrontakis, Maria

doi:10.1038/ijo.2009.187

Cited by 66 publications

(45 citation statements)

References 49 publications

(71 reference statements)

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“…Interestingly, galanin also promotes insulin sensitivity [28,29] . Most recently, our studies in skeletal muscle and adipocytes preliminarily verified the hypothesis that endogenous galanin notably enhances insulin sensitivity and reduces insulin resistance [30,31] .…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, galanin-transgenic mice exhibit increased body weight, visceral adiposity and total serum triglycerides. The obese phenotype of these mice is associated with reduced energy expenditure and insulin resistance [28] . These findings support our previous findings that endogenous galanin contributes to decreased insulin resistance and improved insulin sensitivity in rats [29][30][31] .…”

Section: Effects Of Galanin On Food Intake and Energy Expenditurementioning

confidence: 99%

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Central nervous system regulation of food intake and energy expenditure: role of galanin-mediated feeding behavior

Fang

et al. 2011

Neurosci. Bull.

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Abstract:Galanin is a neuropeptide widely expressed in the brain. It is implicated in energy expenditure, feeding, and the regulation of body weight. Numerous studies have revealed that galanin regulates food intake via galanin receptors, 5-HT 1A receptor and adrenergic α-2 receptor. In this review, we summarize recent findings that reveal the essential role of galanin in increasing food intake as well as body weight and that identify the individual galanin receptor subtypes involved in the brain's modulation of food intake and energy expenditure, to provide a theoretical basis for further studies of different aspects of galanin action.

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Section: Resultsmentioning

confidence: 99%

Section: Effects Of Galanin On Food Intake and Energy Expenditurementioning

confidence: 99%

Central nervous system regulation of food intake and energy expenditure: role of galanin-mediated feeding behavior

Fang

et al. 2011

Neurosci. Bull.

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“…Homozygous galanin-transgenic mice had increased body weight (Poritsanos et al 2009). Infusion of galanin caused a rapid, short, and dose-dependent increase in the blood glucose level (Manabe et al 2003) with elevated sympathetic outflow (Taborsky et al 1999, Kyrkouli et al 2006, although administration of galanin for a long period may reduce the blood glucose level via facilitating GLUT4 translocation and reducing insulin resistance (Zhang et al 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Third, during an oral glucose tolerance test, the galanin concentration in healthy volunteers was positively correlated with blood glucose levels, exhibited a significant increase from time 0 to 90 min, and returned to the basal values at 180 min (Legakis et al 2007). Fourth, galaninknockout mice experienced impaired glucose disposal resulting from a reduction in insulin response and insulin-independent glucose elimination during the glucose tolerance tests (Ahrén et al 2004), while the homozygous galanin transgenic C57BL/6J mice with the obese phenotype showed reduced energy expenditure and enhanced insulin sensitivity (Poritsanos et al 2009). Finally, administration of M35, a galanin antagonist, reduced Glut4 (Slc2a4) mRNA and GLUT4 protein expression levels in the plasma membranes of myocytes and adipocytes, as well as glucose infusion rates in a hyperinsulinemic-euglycemic clamp test, which was a direct assessment of insulin sensitivity in subjects (Guo et al 2011, Liang et al 2012.…”

Section: Introductionmentioning

confidence: 99%

Combined galanin with insulin improves insulin sensitivity of diabetic rat muscles

Yao

Liu

et al. 2014

Journal of Endocrinology

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Although administration of galanin or insulin alone may enhance insulin sensitivity and glucose transporter 4 (GLUT4) trafficking, their cooperative effect on insulin sensitivity is still unclear. In the present study, we evaluated the cooperative effect of both reagents compared with solitary treatment with galanin or insulin in type 2 diabetic rats. Galanin and/or insulin were injected singly or together into type 2 diabetic rats once a day for 15 days. The results indicated that coadministration of both reagents compared with treatment with galanin or insulin alone significantly increased glucose infusion rates in euglycemichyperinsulinemic clamp tests, 2-deoxy-[3 H]D-glucose contents, GLUT4 densities, and pAS160and protein kinase C activity levels, but reduced blood glucose and insulin levels, as well as retinol-binding protein 4 contents, and did not affect Glut4 (Slc2a4) mRNA expression levels in myocytes. The changes in the ratios of GLUT4 immunoreaction in plasma membranes to total cell membranes of myocytes were higher in the coadministrative group compared with either the insulin or the galanin group. These results indicate that cooperation of the two hormones plays a synergic role to improve GLUT4 translocation and insulin sensitivity. This finding indicates the possibility of combining galanin with insulin with the aim of obtaining better antidiabetic efficacy than that of the canonical treatment with insulin alone.

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“…To date three galanin receptors (GalR1, GalR2 and GalR3) have been discovered to be widely distributed in the mammalian central and peripheral nervous system (2). It is acknowledged that galanin has a critical role in the regulation of energy homeostasis (3). Leptin, another adipocyte-derived hormone, is also a key factor in the regulation of body weight and energy expenditure and acts in rodents via hypothalamus receptors to inhibit feeding and increase thermogenesis (4).…”

Section: Introductionmentioning

confidence: 99%

Galanin receptor 2 mediates antifibrogenic effects of galanin on hepatic stellate cells

Zhou

et al. 2016

Experimental and Therapeutic Medicine

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Abstract.Galanin is an endogenous factor involved in the negative regulation of the biological effects of leptin in bioenergetic metabolism. Leptin promotes fibrogenic effects in hepatic stellate cells (HSCs), however, little is known about the effects of galanin on HSCs. In the present study, the biological functions of galanin and its receptors (GalRs) in HSCs were investigated using cell culture in vitro. It was found that galanin and GalR3 mRNA are expressed in quiescent and activated HSCs. GalR2 expression was undetectable in quiescent HSCs but was markedly induced in activated HSCs. In the HSC-T6 cell line, which is an activated rat HSC cell line, treatment with 100 nmol/l galanin significantly inhibited cell proliferation. It also inhibited transforming growth factor (TGF)-β1 and α-smooth muscle actin (SMA) expression and upregulated peroxisome proliferator-activated receptor (PPAR)-γ expression. Following the knockdown of GalR2 by specific small interfering RNA, the activation of GalR3 by galanin does not influence these effects of galanin on HSCs. However, activation of GalR2 alone by galanin following the knockdown of GalR3 inhibits HSC proliferation and TGF-β1 and α-SMA expression, in addition to inducing PPAR-γ expression. These data suggest that galanin inhibits HSC activation and suppresses the profibrogenic features of these cells, and these effects might be mediated by GalR2. Thus, galanin is a potential endogenous factor in the inhibition of liver fibrosis. IntroductionGalanin is a 29-amino acid peptide naturally present in the tissues and fluids of humans and animals (1). To date three galanin receptors (GalR1, GalR2 and GalR3) have been discovered to be widely distributed in the mammalian central and peripheral nervous system (2). It is acknowledged that galanin has a critical role in the regulation of energy homeostasis (3). Leptin, another adipocyte-derived hormone, is also a key factor in the regulation of body weight and energy expenditure and acts in rodents via hypothalamus receptors to inhibit feeding and increase thermogenesis (4). Notably, a previous study confirmed that galanin inhibits leptin expression and secretion in rat adipose tissue and 3T3-L1 adipocytes (5). Leptin has been shown to possess direct profibrogenic activity in the liver, and the absence of leptin is associated with a marked attenuation of the hepatic response to a diverse range of fibrotic stimuli (6). It has been hypothesized that leptin acts directly on hepatic stellate cells (HSCs) to trigger downstream response pathways that ultimately lead to the deposition of extracellular matrix (ECM) (7). However, little is known about the effects of galanin on HSCs. Since the activation and proliferation of HSCs are the key factors in the progress of liver fibrosis, in view of the counteracting effect of galanin on leptin in food intake and energy metabolism, the effect of galanin on the proliferation of HSCs becomes an interesting research topic.It may be hypothesized that galanin is able to inhibit the activation and p...

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Chronic increase of circulating galanin levels induces obesity and marked alterations in lipid metabolism similar to metabolic syndrome

Cited by 66 publications

References 49 publications

Central nervous system regulation of food intake and energy expenditure: role of galanin-mediated feeding behavior

Central nervous system regulation of food intake and energy expenditure: role of galanin-mediated feeding behavior

Combined galanin with insulin improves insulin sensitivity of diabetic rat muscles

Galanin receptor 2 mediates antifibrogenic effects of galanin on hepatic stellate cells

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