Acute high-fat diet paradigms link galanin to triglycerides and their transport and metabolism in muscle

Leibowitz, Sarah F.; Dourmashkin, Jordan; Chang, Guo‐Qing; Hill, James O.; Gayles, Ellis C.; Fried, Susan K.; Wang, Jian

doi:10.1016/j.brainres.2004.02.030

Cited by 78 publications

(111 citation statements)

References 58 publications

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“…This characteristic has been detected in adult OP rats and is likely to be causally related to their propensity toward obesity, rather than a consequence of their over-consuming the high-fat diet which should increase HADH/CS. 13,14 The prepubertal OP rats also exhibited increased expression of the orexigenic peptide GAL in the PVN, similar to results obtained in juvenile OP inbred mice. 34 A recent study in adult rats demonstrates that acute PVN injection of this peptide can reduce the capacity of muscle to metabolize fat, while increasing the metabolism of carbohydrate.…”

Section: Discussionsupporting

confidence: 76%

“…6,7,14,18,[46][47][48][49] They have also been detected in adult OP rats at normal weight, although endogenous NPY, in addition to a suppression, may show no change or even an increase, depending in part on its level of sensitivity to the inhibitory actions of leptin and insulin. [7][8][9]16,50 These findings demonstrate that rats, identified as OP before puberty based on their slightly elevated weight gain, exhibit as adults a typical phenotype associated with obesity.…”

Section: Discussionmentioning

confidence: 99%

“…This is supported by the finding here (Experiment 4) that PVN GAL expression is elevated in prepubertal OP rats in the absence of any change in energy intake or fat pad weights and also by published reports showing that PVN GAL shifts independently of these parameters. 14,44,52 With this peptide particularly responsive to circulating lipids and fat metabolism, it is believed to have a specific function of counteracting the inhibitory actions of dietary fat on carbohydrate balance, 53 which has the ultimate consequence of enhancing weight gain in OP animals.…”

Section: Discussionmentioning

confidence: 99%

“…54,55 While these peptides are known to be inhibited by a rise in leptin or insulin, 56 levels of these hormones were not consistently altered in the prepubertal OP rats of the present study, indicating that they are unlikely to play a major role in producing the reduction in NPY and AgRP. Since these peptides are also known to be suppressed by the consumption of a high-fat diet, 14,57 their role in stimulating the eating, weight gain and body fat accrual of prepubertal OP rats on this energy-rich diet remains unclear. The functions of these peptides are more evident under conditions of negative energy balance, when food is scarce and body weight is reduced.…”

Section: Discussionmentioning

confidence: 99%

“…11,12 While still at normal weight, the OP rats are found to exhibit a phenotype that has similarities to that seen in adult rats after they have become obese. [7][8][9][13][14][15][16] This phenotype in OP animals on a high-fat diet includes a small elevation of insulin, leptin, triglycerides and glucose, reduced sensitivity to insulin and leptin administration, and reduced capacity in muscle to metabolize fat. This is accompanied by an increased expression of the orexigenic peptides, galanin (GAL) in the paraventricular nucleus (PVN) and orexin in the perifornical hypothalamus, which are known to be stimulated by dietary fat and circulating lipids.…”

Section: Introductionmentioning

confidence: 99%

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Weight gain model in prepubertal rats: prediction and phenotyping of obesity-prone animals at normal body weight

et al. 2007

Int J Obes

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Objective: Male Sprague-Dawley rats maintained from birth on a high-fat diet were examined to determine whether a specific measure before puberty can identify and allow one to characterize prepubertal rats at normal weight with high vs low risk for adult obesity. Materials and methods: Measures from weaning (day 21) to around puberty (day 45) were taken of weight gain, absolute body weight and daily energy intake on a high-fat diet and related to the amount of body fat accumulated at maturity (80-100 days of age). Rats identified by a specific prepubertal measure as obesity-prone (OP) vs obesity-resistant (OR) were then characterized before and after puberty. Results: Prepubertal weight gain from days 30 to 35 of age was the strongest and earliest positive correlate of ultimate body fat accrual in adult rats. The highest (8-10 g/day) compared to lowest (5-7 g/day) weight-gain scores identified accurately and reproducibly distinct OP and OR subgroups at day 35 that became obese or remained lean, respectively, as adults. The OP rats with rapid prepubertal weight gain and 50% greater adiposity at maturity (day 100) exhibited the expected phenotype of already-obese rats. These included elevated levels of leptin, insulin, triglycerides and glucose, increased galanin (GAL) peptide levels in the paraventricular nucleus (PVN) and reduced neuropeptide Y (NPY) levels in the arcuate nucleus (ARC). Before puberty (day 35), the OP rats with normal fat pad weights, energy intake and endocrine profile similar to OR rats exhibited these disturbances characteristic of obese rats. They had decreased capacity for fat oxidation in muscle, increased GAL expression in PVN and reduced expression of NPY and agouti-related protein in ARC. Conclusion: Prepubertal weight gain can identify OP rats on day 35 when they have minimal body fat but exhibit specific metabolic and neurochemical disturbances expected to promote obesity and characteristics of already-obese adult rats.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Weight gain model in prepubertal rats: prediction and phenotyping of obesity-prone animals at normal body weight

et al. 2007

Int J Obes

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Not very NICE: deviance, stigma and nutritional guidelines related to healthy weight and obesity

Hann

Frawley

Spedding

2016

Health Planning & Management

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This paper critically examines the current National Institute for Health and Clinical Excellence and National Health Service guidelines on weight management and the avoidance of obesity (NG7). We demonstrate that the guidance is unlikely to produce the desired effect of enabling people to reduce or control their weight through the twin strategies of dieting (primarily using the calories-in, calories-out approach) and increasing their levels of exercise. The paper provides a critical examination of these guidelines and concludes that they are unlikely to encourage maintenance of 'healthy' weights or prevent obesity, are not based upon particularly strong evidence and are misguided in maintaining a persistent focus upon weight rather than other indicators of health. Moreover, we suggest their promotion may produce a number of unintended consequences, including perpetuating body-related stigmatisation and anxieties. Copyright © 2016 John Wiley & Sons, Ltd.

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Galanin and Consummatory Behavior: Special Relationship with Dietary Fat, Alcohol and Circulating Lipids

Barson

Morganstern

Leibowitz

2010

Experientia Supplementum

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Galanin (GAL) plays an integral role in consummatory behavior. In particular, hypothalamic GAL has a positive, reciprocal relationship with dietary fat and alcohol. In this relationship, GAL increases the consumption of fat or alcohol which, in turn, stimulates the expression of GAL, ultimately leading to overconsumption. Through actions in the amygdala, this relationship may become especially important in stress-induced food or drug intake. These effects of GAL in promoting overconsumption may involve various neurotransmitters, with GAL facilitating intake by stimulating norepinephrine and dopamine and reducing satiety by decreasing serotonin and acetylcholine. In addition, GAL in the hypothalamus stimulates the opioid, enkephalin, throughout the brain, which also promotes overconsumption. The relationship between GAL, fat, and alcohol may involve triglycerides, circulating lipids that are released by fat or alcohol and that correlate positively with hypothalamic GAL expression. In females, levels of endogenous GAL also fluctuate across the reproductive cycle, driven by a rise in the ovarian steroids, estrogen, and progesterone. They peak during the proestrous phase and also at puberty, simultaneous to a sharp increase in preference for fat to meet energy demands. Prenatal exposure to a high-fat diet also enhances hypothalamic expression of GAL into adulthood because of an increase in neurogenesis and proliferation of GAL-expressing neurons in this region. This organizational change may reflect the role of GAL in neuronal development, including neurite growth in adulthood, cell survival in aging, and cell stability in the disease state. By responding positively to fat and alcohol and guiding further neuronal development, GAL potentiates a long-term propensity to overconsume fat and alcohol.

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Acute high-fat diet paradigms link galanin to triglycerides and their transport and metabolism in muscle

Cited by 78 publications

References 58 publications

Weight gain model in prepubertal rats: prediction and phenotyping of obesity-prone animals at normal body weight

Weight gain model in prepubertal rats: prediction and phenotyping of obesity-prone animals at normal body weight

Not very NICE: deviance, stigma and nutritional guidelines related to healthy weight and obesity

Galanin and Consummatory Behavior: Special Relationship with Dietary Fat, Alcohol and Circulating Lipids

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