Modifications in food intake and energy metabolism in rats as a function of chronic naltrexone infusions

Marks-Kaufman, Robin; Bal'magiya, T. A.; Gross, Erica R.

doi:10.1016/0091-3057(84)90016-9

Cited by 63 publications

(37 citation statements)

References 19 publications

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“…These findings contrast with those of naloxone and naltrexone treatment, which require significantly higher doses or parenteral administration (20,22,33). The actions of LY255582 were mediated through occupancy of opioid receptors as demonstrated by ex vivo receptor binding.…”

Section: Discussioncontrasting

confidence: 52%

“…Moreover, endogenous opioid peptides (␤-endorphin, the enkephalins, and dynorphin) are elevated in obesity and by fasting (6,9,14,21,44). Numerous studies using antagonists to opioid receptors report reduced food intake and body weight in rodents (1,17,21,22,33,38,39). Interestingly, the inhibitory effects of opioid receptor antagonists on food intake and body weight appear most pronounced in obese animals or when animals are fed a highly palatable diet (12,19).…”

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confidence: 99%

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Antagonism of opioid receptors reduces body fat in obese rats by decreasing food intake and stimulating lipid utilization

Statnick

Tinsley

Eastwood

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Agonists to opioid receptors induce a positive energy balance, whereas antagonists at these receptors reduce food intake and body weight in rodent models of obesity. An analog of 3,4-dimethyl-4-(3-hydroxyphenyl)piperidine, LY255582, is a potent non-morphinan antagonist for μ-, κ-, and δ-receptors ( K i of 0.4, 2.0, and 5.2 nM, respectively). In the present study, we examined the effects of oral LY255582 treatment on caloric intake, calorie expenditure, and body composition in dietary-induced obese rats. Acute oral treatment of LY255582 produced a dose-dependent decrease in energy intake and respiratory quotient (RQ), which correlated with the occupancy of central opioid receptors. Animals receiving chronic oral treatment with LY255582 for 14 days maintained a negative energy balance that was sustained by increased lipid use. Analysis of body composition revealed a reduction in fat mass accretion, with no change in lean body mass, in animals treated with LY255582. Therefore, chronic treatment with LY255582 reduces adipose tissue mass by reducing energy intake and stimulating lipid use.

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Section: Discussioncontrasting

confidence: 52%

mentioning

confidence: 99%

Antagonism of opioid receptors reduces body fat in obese rats by decreasing food intake and stimulating lipid utilization

Statnick

Tinsley

Eastwood

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It has been suggested that opioids favor the conservation of energy because the weight reduction induced by opioid antagonists in rats fed an adipogenic diet exceeded the degree to which caloric intake was reduced (6,24). However, controversial results on energy expenditure have been obtained with pharmacological tools (6,7). Two studies have reported that nonselective opioid antagonists induce a decrease in RQ, thereby indicating an opioid modulation of lipid oxidation, in rats fed regular and high-fat diets (7,8).…”

Section: Discussionmentioning

confidence: 99%

“…However, controversial results on energy expenditure have been obtained with pharmacological tools (6,7). Two studies have reported that nonselective opioid antagonists induce a decrease in RQ, thereby indicating an opioid modulation of lipid oxidation, in rats fed regular and high-fat diets (7,8). However, RQ decreases with reductions in caloric intake (8), and it has not been possible thus far to separate the feeding and metabolic effects of opioids by pharmacological manipulation.…”

Section: Discussionmentioning

confidence: 99%

Resistance to Diet-Induced Obesity in μ-Opioid Receptor–Deficient Mice

et al. 2005

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Using pharmacological tools, a role for opioid receptors in the regulation of food intake has been documented. However, the involvement of specific receptor subtypes remains questionable, and little information is available regarding a role for opioid receptors in energy metabolism. Using adult male mice lacking the -opioid receptor (MOR) gene (MOR ؊/؊ ), we show that the MOR is not essential for the maintenance of normal levels of ad libitum food intake but does modulate the efficiency of energy storage during high-fat diets through the regulation of energy partitioning. When fed a regular diet, MOR ؊/؊ mice displayed only subtle alterations in energy homeostasis, suggesting a relative overuse of fat as a fuel source in the fed state. When fed a high-fat diet, MOR ؊/؊ mice were resistant to obesity and impaired glucose tolerance, despite having similar energy intake to wild-type mice. This resistance to obesity was associated with a strong induction of the expression of key mitochondrial enzymes involved in fatty acid oxidation within skeletal muscle. This metabolic role of the MOR, which is consistent with the properties of a "thrifty gene," suggests that the MOR pathway is a potential target for pharmacological intervention in the treatment of obesity associated with the intake of fatty diets. Diabetes 54: 3510 -3516, 2005 T he endogenous opioid system encompasses cloned receptor populations (, ␦, and ) and ligands (␤-endorphin, the enkephalins, and the dynorphins). Extensive work indicates that the opioid system plays a role in the regulation of appetite. Opioid receptors and peptides are expressed in sites of the central nervous system that play a role in regulating feeding behavior, and pharmacological experiments using opioid receptor ligands show that agonists promote eating and antagonists decrease food intake, at least in the short term (1-3). Numerous pharmacological studies indicate that opioids also play a role in modulating the rewarding effects of food (3-5). In contrast, little information suggests that opioids have a role in energy metabolism (6 -8).The need to establish the specific role of the opioid receptors in energy homeostasis has led to studies using putative specific opioid receptor ligands or, more recently, antisense probes directed against specific exons of opioid receptor genes (3,9). Pharmacological studies suggest that the and pathways are part of an interconnected brain network and participate in the orexigenic effect of several peptides that regulate food intake (10 -13). However, the interpretation of these data is complicated by our poor knowledge of the in vivo selectivity of ligand-receptor interactions that have been established in vitro (9,14).Recent studies conducted in mutant mice null for the opioid receptors have complemented pharmacological approaches and clarified the role of each receptor in nociception, anxiety, and drug abuse (14). To further define the role of the -opioid receptor (MOR) pathway in energy homeostasis, we characterized mice lacking the MOR gene ...

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“…Although opioid agonists and antagonists can affect the intakes of normal foods at higher doses or when those foods are presented alone, their effects are more pronounced on foods that rate higher in palatability, such as those high in fat or rich in carbohydrates [34][35][36][37][38]. It has been then suggested the EOS is likely responsible for regulating intakes of particular macronutrients [39][40][41]. However, further studies have found that what seems to be important is not a specific macronutrient, but rather the baseline preference of the animal [42][43][44].…”

Section: Introductionmentioning

confidence: 99%

Opioidergic and dopaminergic modulation of cost/benefit decision-making in Long Evans Rats

Morales

Currie

Hackenberg

et al. 2017

Physiology & Behavior

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Highlights• We assess opioid and dopamine control of food intake with two cost/benefit decision-making tasks • Naloxone reduces operant responses for palatable food without affecting free chow intake • Haloperidol shifts behavior away from lever pressing and increases free chow feeding • Naloxone reduces preference for palatable banana pellets when no effort is involved • Dopamine antagonism reduces intake of both foods without altering preference AbstractEating disorders are associated with impaired decision-making and dysfunctional reward-related neurochemistry. The present study examined the potential contributions of dopamine and opioid signaling to these processes using two different decision-making tasks. In one task, Long Evans Rats chose between working for a preferred food (high-carbohydrate banana-flavored sucrose pellets) by lever pressing on a progressive-ratio schedule of reinforcement vs. obtaining less preferred laboratory chow that was concurrently available. In a second (effort-free) task, rats chose between the same two reinforcers when they were both available freely. Rats were trained in these tasks before receiving haloperidol (0.00, 0.05, 0.10 mg/kg, intraperitoneally (i.p.)) or naloxone (0.0, 1.5, 3.0 mg/kg, i.p.). In the first task, haloperidol decreased breakpoint, lever presses, number of reinforcers earned, and increased chow intake, whereas naloxone decreased breakpoint and number of reinforcers earned but had no effect on chow consumption. In the effort-free task, haloperidol reduced intakes of both foods without affecting preference, whereas naloxone selectively reduced the consumption of banana-pellets. The present findings support converging evidence suggesting that DA signaling affects processes more closely related to appetitive motivation, leaving other components of motivation unchanged. By contrast, opioid signaling appears to mediate aspects of hedonic feeding by selectively altering intakes of highly palatable foods. For preferred foods, both appetitive and consummatory aspects of food intake were altered by opioid receptor antagonism. Our findings argue against a general suppression of appetite by either compound, as appetite manipulations have been shown to unselectively alter intakes of both types of food regardless of the task employed.

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Modifications in food intake and energy metabolism in rats as a function of chronic naltrexone infusions

Cited by 63 publications

References 19 publications

Antagonism of opioid receptors reduces body fat in obese rats by decreasing food intake and stimulating lipid utilization

Antagonism of opioid receptors reduces body fat in obese rats by decreasing food intake and stimulating lipid utilization

Resistance to Diet-Induced Obesity in μ-Opioid Receptor–Deficient Mice

Opioidergic and dopaminergic modulation of cost/benefit decision-making in Long Evans Rats

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