Chronic food restriction and acute food deprivation decrease mRNA levels of opioid peptides in arcuate nucleus

1996 ◽  
Vol 270 (5) ◽  
pp. R1019-R1024 ◽  
Author(s):  
E. M. Kim ◽  
C. C. Welch ◽  
M. K. Grace ◽  
C. J. Billington ◽  
A. S. Levine
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Food Deprivation ◽  
Food Restriction ◽  
Arcuate Nucleus ◽  
Mrna Levels ◽  
Endogenous Opioid ◽  
Pomc Mrna ◽  
Opioid Administration ◽  
Ad Libitum Intake

Although opioid administration induces food intake, the relationship between endogenous opioid synthesis and food consumption is unclear. Two studies examined the effects of food restriction and deprivation on opioid mRNA levels in the arcuate nucleus (ARC) of the rat. Body weight significantly decreased following food restriction and deprivation (P < 0.0001). In experiment 1, food restriction of 10,20,30, and 40% (g) of ad libitum intake for 14 days decreased proDynorphin (proDyn), proEnkephalin (proEnk), and proOpiomelanocortin (POMC) mRNA levels in a linear fashion relative to changes in body weight (r = 0.398, P = 0.0011; r = 0.455, P = 0.0028; r = 0.292, P = 0.0642, respectively). In experiment 2, 48 h deprivation significantly decreased mRNA levels of proDyn and POMC by 23.7% (P < 0.05) and 45.6% (P < 0.01), respectively, whereas 24 h food deprivation decreased POMC mRNA by 43.% (P < 0.01). proEnk mRNA was not affected by 24- or 48-h food deprivation. Restricting food intake suppressed mRNA levels of proDyn, proEnk, and POMC by 29.7, 22.3, and 44.4%, respectively, in 20% restricted rats and by 35.5, 26.8, and 45.6%, respectively, in 40%restricted rats (P < 0.01). It appears that ARC mRNA levels of proDyn, proEnk, and POMC are directly related to the amount of food consumed and/or changes in body weight in food-restricted and food-deprived rats.

Acute food deprivation and chronic food restriction differentially affect hypothalamic NPY mRNA expression

2003 ◽  
Vol 285 (5) ◽  
pp. R1030-R1036 ◽  
Author(s):  
Sheng Bi ◽  
Benjamin M. Robinson ◽  
Timothy H. Moran
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Food Deprivation ◽  
Food Restriction ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Body Weight Loss ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Chronic Food Restriction

Although acute food deprivation and chronic food restriction both result in body weight loss, they produce different metabolic states. To evaluate how these two treatments affect hypothalamic peptide systems involved in energy homeostasis, we compared patterns of hypothalamic neuropeptide Y (NPY), agouti-related protein (AgRP), proopiomelanocotin (POMC), and leptin receptor gene expression in acutely food-deprived and chronically food-restricted rats. Both acute food deprivation and chronic food restriction reduced body weight and circulating leptin levels and resulted in increased arcuate NPY and decreased arcuate POMC gene expression. Arcuate AgRP mRNA levels were only elevated in acutely deprived rats. NPY gene expression was increased in the compact subregion of the dorsomedial hypothalamus (DMH) in response to chronic food restriction, but not in response to acute food deprivation. Leptin receptor expression was not affected by either treatment. Double in situ hybridization histochemistry revealed that, in contrast to the situation in the arcuate nucleus, NPY and leptin receptor mRNA-expressing neurons were not colocalized in the DMH. Together, these data suggest that arcuate and DMH NPY gene expression are differentially regulated. DMH NPY-expressing neurons do not appear to be under the direct control of leptin signaling.

Naltrexone induces arcuate nucleus neuropeptide Y gene expression in the rat

1996 ◽  
Vol 271 (1) ◽  
pp. R289-R294 ◽  
Author(s):  
C. M. Kotz ◽  
M. K. Grace ◽  
J. E. Briggs ◽  
C. J. Billington ◽  
A. S. Levine
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Food Deprivation ◽  
Arcuate Nucleus ◽  
Uncoupling Protein ◽  
Endogenous Opioids ◽  
Brown Fat ◽  
Mrna Levels ◽  
Sprague Dawley

Neuropeptide Y (NPY) has potent effects on several components of energy metabolism, including increased feeding and decreased brown fat thermogenesis. Negative energy balance, such as food deprivation, increases NPY mRNA in hypothalamic arcuate nucleus (ARC). Naltrexone (NLTX), an opioid receptor antagonist, decreases NPY-induced feeding. We hypothesized that NLTX would alter ARC NPY mRNA and change NPY effects on brown fat. Osmotic minipumps prefilled with either saline or NLTX (70 micrograms/h) were implanted subcutaneously in 32 male Sprague-Dawley rats. One-half of the rats were food deprived and one-half were allowed food ad libitum for 48 h. Food intake was measured at 24 and 48 h. At 48 h, ARC NPY mRNA and brown fat uncoupling protein (UCP) mRNA levels were determined using cDNA probes. Forty-eight-hour food intake was significantly decreased by 24% after NLTX infusion. Food deprivation and NLTX treatment significantly and independently increased ARC NPY mRNA and decreased UCP mRNA levels in brown fat, suggesting a complex interaction between hypothalamic NPY and endogenous opioids in the regulation of energy balance.

Behavioral, endocrine, and hypothalamic responses to involuntary overfeeding

1996 ◽  
Vol 271 (3) ◽  
pp. R819-R823 ◽  
Author(s):  
R. J. Seeley ◽  
C. A. Matson ◽  
M. Chavez ◽  
S. C. Woods ◽  
M. F. Dallman ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Paraventricular Nucleus ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Arcuate Nucleus ◽  
Negative Energy ◽  
Per Se ◽  
Underlying Mechanisms

The suppression of food intake after a period of forced overfeeding is potent and long lasting, yet little is known of the underlying mechanisms for this regulatory response. Rats were overfed via a surgically implanted gastrostomy tube. During overfeeding, plasma insulin and corticotropin-releasing hormone (CRH) mRNA in the paraventricular nucleus of the hypothalamus were elevated compared with controls and with overfed rats allowed 3 days to recover from the overfeeding regimen such that body weight returned to the level of controls. In contrast, rats that were not overfed but were pair-fed to the low spontaneous food intake of previously overfed rats lost weight and had significantly reduced plasma insulin and elevated mRNA for neuropeptide Y (NPY) in the arcuate nucleus of the hypothalamus. The results indicate that overfeeding produces an activation of hypothalamic CRH system that may contribute to the hypophagia that accompanies involuntary overfeeding. Furthermore, the hypothalamic NPY response to food restriction is not tied to low food intake per se, but rather to negative energy balance.

scholarly journals Antiobesity Effects of the β-Cell Hormone Amylin in Diet-Induced Obese Rats: Effects on Food Intake, Body Weight, Composition, Energy Expenditure, and Gene Expression

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5855-5864 ◽  
Author(s):  
Jonathan D. Roth ◽  
Heather Hughes ◽  
Eric Kendall ◽  
Alain D. Baron ◽  
Christen M. Anderson
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Respiratory Quotient ◽  
Metabolic Effects ◽  
Mrna Levels ◽  
Lean Tissue ◽  
Reduced Body ◽  
Diet Induced Obesity ◽  
Cell Hormone

Effects of amylin and pair feeding (PF) on body weight and metabolic parameters were characterized in diet-induced obesity-prone rats. Peripherally administered rat amylin (300 μg/kg·d, 22d) reduced food intake and slowed weight gain: approximately 10% (P &lt; 0.05), similar to PF. Fat loss was 3-fold greater in amylin-treated rats vs. PF (P &lt; 0.05). Whereas PF decreased lean tissue (P &lt; 0.05 vs. vehicle controls; VEH), amylin did not. During wk 1, amylin and PF reduced 24-h respiratory quotient (mean ± se, 0.82 ± 0.0, 0.81 ± 0.0, respectively; P &lt; 0.05) similar to VEH (0.84 ± 0.01). Energy expenditure (EE mean ± se) tended to be reduced by PF (5.67 ± 0.1 kcal/h·kg) and maintained by amylin (5.86 ± 0.1 kcal/h·kg) relative to VEH (5.77 ± 0.0 kcal/h·kg). By wk 3, respiratory quotient no longer differed; however, EE increased with amylin treatment (5.74 ± 0.09 kcal/·kg; P &lt; 0.05) relative to VEH (5.49 ± 0.06) and PF (5.38 ± 0.07 kcal/h·kg). Differences in EE, attributed to differences in lean mass, argued against specific amylin-induced thermogenesis. Weight loss in amylin and pair-fed rats was accompanied by similar increases arcuate neuropeptide Y mRNA (P &lt; 0.05). Amylin treatment, but not PF, increased proopiomelanocortin mRNA levels (P &lt; 0.05 vs. VEH). In a rodent model of obesity, amylin reduced body weight and body fat, with relative preservation of lean tissue, through anorexigenic and specific metabolic effects.

scholarly journals The Effect of a 2-Week Red Ginseng Supplementation on Food Efficiency and Energy Metabolism in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1726
Author(s):  
Hyejung Hwang ◽  
Jisu Kim ◽  
Kiwon Lim
Keyword(s):  
Body Weight ◽  
Energy Metabolism ◽  
Food Intake ◽  
Weight Control ◽  
Fat Oxidation ◽  
Substrate Utilization ◽  
Mrna Levels ◽  
Red Ginseng ◽  
Energy Substrate ◽  
Metabolism Regulation

Red ginseng (RG) ingestion reportedly affects body weight, food intake, and fat accumulation reduction. It also induces changes in energy metabolism regulation and glycemic control. Previously, 2-week RG ingestion with endurance training was found to enhance fat oxidation during exercise. However, such effects on energy metabolism and the expression of mRNAs related to energy substrate utilization in resting mice (untrained mice) are still unclear. Here, we determined the effect of RG on energy metabolism and substrate utilization in untrained male mice. Twenty-four mice were separated into an RG group that received a daily dosage of 1 g/kg RG for 2 weeks, and a control (CON). Energy expenditure, blood and tissue glycogen levels, and expression of mRNAs related to energy substrate utilization in muscles were measured before and 2 weeks after treatment. Total food intake was significantly lower in the RG than in the CON group (p < 0.05), but final body weights did not differ. Carbohydrate and fat oxidation over 24 h did not change in either group. There were no significant differences in gastrocnemius GLUT4, MCT1, MCT4, FAT/CD36, and CPT1b mRNA levels between groups. Thus, the effects of RG ingested during rest differ from the effects of RG ingestion in combination with endurance exercise; administering RG to untrained mice for 2 weeks did not change body weight and energy metabolism. Therefore, future studies should consider examining the RG ingestion period and dosage for body weight control and improving energy metabolism.

Expression of FAS within hypothalamic neurons: a model for decreased food intake after C75 treatment

2002 ◽  
Vol 283 (5) ◽  
pp. E867-E879 ◽  
Author(s):  
Eun-Kyoung Kim ◽  
Ian Miller ◽  
Leslie E. Landree ◽  
Felice F. Borisy-Rudin ◽  
Pierre Brown ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Fatty Acid Synthase ◽  
Arcuate Nucleus ◽  
Potent Inhibitor ◽  
Brain Regions ◽  
Axon Terminals ◽  
Paraventricular Nuclei ◽  
Brain Expression

We previously demonstrated that C75, a specific and potent inhibitor of fatty acid synthase (FAS), reduced food intake and decreased body weight in mice. In the present study, we determined that these effects were not due to conditioned taste aversion. To investigate the mechanism of C75 action, we examined FAS brain expression. FAS was expressed in a number of brain regions, including arcuate and paraventricular nuclei (PVN) within regions that comprise the arcuate-PVN pathway in mouse and human. Although C75 and fasting significantly downregulated liver FAS, FAS levels remained high in hypothalamus, indicating that FAS levels were regulated differently in brain from those in liver. Double fluorescence in situ for FAS and neuropeptide Y (NPY) showed that FAS co-localized with NPY in neurons in the arcuate nucleus. NPY immnuoreactivity after C75 treatment was decreased in axon terminals that innervate the PVN and lateral hypothalamus. Collectively, these results demonstrate that FAS is present and active in neurons and suggests that C75 may alter food intake via interactions within the arcuate-PVN pathway mediated by NPY.

Additive effects of lactation and food restriction to increase hypothalamic neuropeptide Y mRNA in rats

1997 ◽  
Vol 152 (3) ◽  
pp. 365-369 ◽  
Author(s):  
J P H Wilding ◽  
M O Ajala ◽  
P D Lambert ◽  
S R Bloom
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Food Restriction ◽  
Mrna Levels ◽  
Additive Effects ◽  
Daily Food Intake ◽  
Glucose Levels ◽  
Daily Food ◽  
Pregnancy And Lactation ◽  
Effect Of Food

Neuropeptide Y (NPY) is the most powerful appetite stimulant known, and rates of synthesis and release in the hypothalamus correlate closely with nutritional status. Pregnancy and lactation provide an excellent model of physiological hyperphagia. In this study the authors measured food intake, plasma glucose, insulin and luteinizing hormone (LH) and hypothalamic NPY mRNA in rats during pregnancy and in early and late lactation. The effect of food restriction (to 80% of control) during lactation was also studied. Pregnancy resulted in a modest increase in daily food intake over non-lactating controls (controls: 15·6±0·6 g, pregnant: 19·8±1·1 g, P<0·01) During lactation food intake increased dramatically to 355% of non-lactating levels by the 12th day. Insulin and glucose levels were unchanged in lactation, except in the food-restricted animals, when insulin levels were reduced to 49·5±18·4 pmol/l compared with 215±55 pmol/l (P<0·01) in lactating, non-restricted animals, and glucose was reduced to 3·7±0·2 mmol/l compared with 5·1 ± 0·2 mmol/l in non-restricted lactating animals. Hypothalamic NPY mRNA was unchanged in pregnancy, moderately increased after 5 days lactation (130±6·2% of control, P<0·01) and increased further at 14 days lactation (179 ± 14%, P<0·001). The greatest changes occurred in the animals who were food-deprived during lactation, when hypothalamic NPY mRNA levels reached 324 ± 44% (P<0·001) of non-lactating levels. Increases in hypothalamic NPY synthesis may be partly responsible for the increase in food intake seen in lactation, but unlike in food deprivation, the increase is not related to circulating insulin, suggesting involvement of other regulatory factors. Journal of Endocrinology (1997) 152, 365–369

scholarly journals Gonadotropin-Releasing Hormone-II Messenger Ribonucleic Acid and Protein Content in the Mammalian Brain Are Modulated by Food Intake

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5069-5077 ◽  
Author(s):  
Alexander S. Kauffman ◽  
Karolina Bojkowska ◽  
Aileen Wills ◽  
Emilie F. Rissman
Keyword(s):  
Food Intake ◽  
Food Restriction ◽  
Mammalian Brain ◽  
Mrna Levels ◽  
Female Reproduction ◽  
Messenger Ribonucleic Acid ◽  
Medial Habenula ◽  
Sufficient Energy ◽  
Peptide Family ◽  
Ad Libitum

GnRH-II is the most evolutionarily conserved member of the GnRH peptide family. In mammals, GnRH-II has been shown to regulate reproductive and feeding behaviors. In female musk shrews, GnRH-II treatment increases mating behaviors and decreases food intake. Although GnRH-II-containing neurons are known to reside in the midbrain, the neural sites of GnRH-II action are undetermined, as is the degree to which GnRH-II is regulated by energy availability. To determine whether GnRH-II function is affected by changes in food intake, we analyzed the levels of GnRH-II mRNA in the midbrain and GnRH-II protein in numerous target regions. Adult musk shrews were ad libitum fed, food restricted, or food restricted and refed for varying durations. Compared with ad libitum levels, food restriction decreased, and 90 min of refeeding reinstated, GnRH-II mRNA levels in midbrain and GnRH-II peptide in several target areas including the medial habenula and ventromedial nucleus. Refeeding for 90 min also reinstated female sexual behavior in underfed shrews. In male shrews, abundant GnRH-II peptide was present in all sites assayed, including the preoptic area, a region with only low GnRH-II in females. In contrast to females, food restriction did not affect GnRH-II protein in male brains or inhibit their mating behavior. Our results further define the relationship between GnRH-II, energy balance, and reproduction, and suggest that food restriction may inhibit female reproduction by reducing GnRH-II output to several brain nuclei. We postulate that this highly conserved neuropeptide functions similarly in other mammals, including humans, to fine-tune reproductive efforts with periods of sufficient energy resources.

scholarly journals Serotonin 5-HT2C Receptor Agonist Promotes Hypophagia via Downstream Activation of Melanocortin 4 Receptors

Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1323-1328 ◽  
Author(s):  
Daniel D. Lam ◽  
Magdalena J. Przydzial ◽  
Simon H. Ridley ◽  
Giles S. H. Yeo ◽  
Justin J. Rochford ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Arcuate Nucleus ◽  
Weight Percent ◽  
Ingestive Behavior ◽  
The Novel ◽  
Functional Importance ◽  
Serotonin 2C Receptor ◽  
Pomc Mrna ◽  
Melanocortin 4 Receptor

The neurotransmitter serotonin (5-hydroxytryptamine) is a well-established modulator of energy balance. Both pharmacological and genetic evidence implicate the serotonin 2C receptor (5-HT2CR) as a critical receptor mediator of serotonin’s effects on ingestive behavior. Here we characterized the effect of the novel and selective 5-HT2CR agonist BVT.X on energy balance in obese and lean mice and report that BVT.X significantly reduces acute food intake without altering locomotor activity or oxygen consumption. In an effort to elucidate the mechanism of this effect, we examined the chemical phenotype of 5-HT2CR-expressing neurons in a critical brain region affecting feeding behavior, the arcuate nucleus of the hypothalamus. We show that 5-HT2CRs are coexpressed with neurons containing proopiomelanocortin, known to potently affect appetite, in the arcuate nucleus of the hypothalamus of the mouse. We then demonstrate that prolonged infusion with BVT.X in obese mice significantly increases Pomc mRNA and reduces body weight, percent body fat, and initial food intake. To evaluate the functional importance of melanocortin circuitry in the effect of BVT.X on ingestive behavior, we assessed mice with disrupted melanocortin pathways. We report that mice lacking the melanocortin 4 receptor are not responsive to BVT.X-induced hypophagia, demonstrating that melanocortins acting on melanocortin 4 receptor are a requisite downstream pathway for 5-HT2CR agonists to exert effects on food intake. The data presented here not only indicate that the novel 5-HT2CR agonist BVT.X warrants further investigation as a treatment for obesity but also elucidate specific neuronal pathways potently affecting energy balance through which 5-HT2CR agonists regulate ingestive behavior.

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