Neuroendocrine Profiles in Galanin-Overexpressing and Knockout Mice

Hohmann, John G.; Krasnow, Stephanie M.; Teklemichael, Dawit N.; Clifton, Donald K.; Wynick, David; Steiner, Robert A.

doi:10.1159/000071308

Cited by 57 publications

(44 citation statements)

References 35 publications

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“…This latter finding is consistent with the phenotype reported for the GKO mouse, which is more sensitive to leptin treatment [38] . These results correspond with previous reports that GKO mice have significant alterations in neuroendocrine homeostasis [26] , suggesting that through GalR1, galanin is involved in conditioned neuroendocrine homeostasis. Notably, in contrast to an acute high-fat diet, GalR1-KO mice with a chronic highfat diet consume less food and daily energy, indicating that GalR1 may oppose positive energy-balance [35] .…”

Section: Effects Of Galanin On Food Intake and Energy Expendituresupporting

confidence: 92%

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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: Effects Of Galanin On Food Intake and Energy Expendituresupporting

confidence: 92%

“…The complete loss of galanin in GKO mice leads to significant alterations in neuroendocrine homeostasis, whereas targeted overexpression of galanin in the brain does not interfere with normal neuroendocrine function [26] .…”

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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“…This is supported by evidence that acute injection of GAL has a stronger feeding-stimulatory effect on a high-fat diet compared with a low-fat diet, and it has metabolic effects that include a reduction in energy expenditure and sympathetic nervous system activity and a stimulation of carbohydrate over fat metabolism (29,36,38,42,72). Also, chronic GAL injection increases body weight and body fat accrual, most strongly on a high-fat diet (23,72).…”

Section: Discussionmentioning

confidence: 85%

Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet

Leibowitz¹,

Chang²,

Dourmashkin³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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. Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet. Am J Physiol Endocrinol Metab 290: E258 -E267, 2006; doi:10.1152/ajpendo.00609.2004.-The objective of this study was to investigate meal-related endocrine changes that permit one to identify Sprague-Dawley rats at normal weight that are prone (OP) vs. resistant (OR) to obesity. In blood collected via chronic cardiac catheters, a 2-h high-fat meal (HFM, 50% fat, 40 kcal) at dark onset caused a significant increase in leptin, insulin, and triglycerides compared with premeal levels. Similar to patterns in already obese compared with lean rats on a high-fat diet, these meal-induced endocrine changes in normalweight rats on lab chow were almost twofold larger in OP rats that, compared with OR rats, subsequently accumulated 100% more fat mass on a chronic high-fat diet. These exaggerated endocrine changes were similarly observed in blood collected using a simpler tail vein puncture procedure. In three separate experiments, the HFM-induced rise in leptin was found to be the strongest, positive correlate (r ϭ ϩ0.58, ϩ0.62 and ϩ0.64) of long-term body fat accrual. The lowest (2-5 ng/ml) vs. highest (6 -9 ng/ml) scores for this post-HFM leptin measurement identified distinct OR and OP subgroups, respectively, when they were similar in body weight (340 -350 g), premeal leptin (2.6 -3.4 ng/ml), and meal size (40 kcal). Subsequent tests in these normal-weight OP rats revealed a distinct characteristic compared with OR rats, namely, exaggerated HFM-induced rise in expression of the orexigenic peptide galanin in the paraventricular nucleus. Thus, with this HFM-induced leptin measurement, OP rats can be identified while still at normal weight and then investigated for mechanisms that contribute to their excessive body fat accrual on a high-fat diet.insulin; triglycerides; galanin; neuropeptide Y OBESITY IS A COMPLEX DISORDER with multiple etiologies. To identify factors that cause or contribute to the development of obesity, it is essential to establish markers of susceptibility in individual subjects before the onset of this disorder. By identifying "obesity-resistant" (OR) and "obesity-prone" (OP) animals at normal body weight, studies can then be performed to characterize disturbances that precede and possibly promote the obesity. Investigations in inbred mouse or rat strains with differential propensities toward obesity have been informative (4,55,69). However, detailed studies of these populations at young ages, before they become different in their body weight, are still lacking. Reports in rats that have been selectively bred on the basis of their differential weight gain on a high-calorie diet (31, 34) hold particular promise in revealing the phenotype of OP rats at normal weight. These selectively bred animals deserve far more attention than they have received to date.

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“…This is supported by evidence that the effects induced by galanin, a stimulation of food intake, body weight and body fat accrual, are stronger in animals consuming a fat-rich diet. 18,[37][38][39][40][41] Galanin on a high-fat diet may contribute to the higher weight gain of these obesity-prone mice through various metabolic effects, including a reduction in energy expenditure and sympathetic nervous system activity. 42,43 The results obtained in the C57BL/6J mice, which differ from the AKR/J and DBA/2J, argue against a major role for galanin and circulating lipids in this strain.…”

Section: 20mentioning

confidence: 99%

Distinct phenotypes of obesity-prone AKR/J, DBA2J and C57BL/6J mice compared to control strains

et al. 2005

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Objective: To characterize and compare three obesity-prone inbred strains, AKR/J, DBA/2J and C57BL/6J, to three control strains, C3H/HeJ, BALB/cByJ and C57L/J, selected based on their normal eating patterns and moderate weight gain on highcalorie diets. Methods and procedures: These six strains were examined at 5 weeks of age while still of normal body weight, and they were maintained for 1 day or 3 weeks on different feeding paradigms with macronutrient diets. Measurements were taken of macronutrient intake, body weight and body fat accrual, circulating hormones and metabolites, and the hypothalamic peptide, galanin. Results: The three control strains each selected a balanced diet with 50% carbohydrate and 15-25% fat when given a choice of macronutrients, and they had similar, normal range of scores for the measures of body weight, adiposity, the hormones, insulin and leptin, and the metabolites, glucose and triglycerides. When compared to this control baseline, the obesity-prone strains with similar total caloric intake to controls selected a diet with significantly more fat (30-40%) and less carbohydrate (o40%). They also had greater adiposity, with the largest differences detected for the AKR/J and DBA/2J strains. These two obesity-prone strains compared to control strains had elevated levels of insulin and leptin. They also had higher triglyceride levels and increased expression and levels of galanin in the hypothalamic paraventricular nucleus. A very different pattern was detected in the obesity-prone C57BL/6J strain, which exhibited a stronger preference for protein as well as fat, normal levels of insulin, leptin and triglycerides, hyperglycemia relative to all other strains, and a small increase in galanin. Conclusion: These comparisons to control strains revealed a distinct phenotype in the two obesity-prone strains, AKR/J and DBA/2J, which is very similar to that described in obesity-prone, outbred rats. They also identified a clearly different phenotype in the obesity-prone C57BL/6J strain.

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Neuroendocrine Profiles in Galanin-Overexpressing and Knockout Mice

Cited by 57 publications

References 35 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

Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet

Distinct phenotypes of obesity-prone AKR/J, DBA2J and C57BL/6J mice compared to control strains

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