IThe effects of ,-adrenoceptor blockade on the metabolic responses to isoprenaline have been studied in an in vitro system of isolated fat cells and in six normal subjects. 2 The inhibitory effects of varying concentrations of acebutolol, practolol and propranolol on free fatty acid (FFA) release produced by isoprenaline (10-7 M) were compared in isolated fat cells prepared from rat epididymal adipose tissue. Acebutolol and practolol, at equimolar concentrations, showed a similar inhibitory effect whilst propranolol was approximately 100 times more potent then either drug. At 10-SM concentration of propranolol, lipolysis was virtually abolished whilst at the same molar concentration, acebutolol and practolol halved the response.3 Six healthy volunteers received three successive 15 min intravenous isoprenaline challenges (0.03 ,g kg-' min-' ) per individual experiment. The first acted as a control whilst the following two were given either after single oral doses of placebo, acebutolol or practolol. The mean (± s.e. mean) basal FFA level was 0.77 ± 0.06 mEq/1 and subsequent resting values after the administration of placebo or ,-adrenoceptor blocker were not significantly different. 4 Acebutolol inhibited the respective mean rises in FFA, produced by both post-control isoprenaline challenges, by (mean ± s.e. mean) 70 ± 4% and 84 ± 5%. The comparable figures for practolol were 33 ± 15% and 24 ± 20%. The higher serum concentration of acebutolol produced greater inhibition but correlation of log serum concentration of the drug with percentage inhibition of FFA rise did not achieve significance. 5 Administration of isoprenaline, acebutolol or practolol did not significantly alter serum glucose, triglyceride or cholesterol levels. 6 Acebutolol and practolol effectively blocked the isoprenaline-induced tachycardia. The degree of blockade produced by practolol was greater than its inhibitory effect on FFA release. The diastolic fall in blood pressure in response to isoprenaline was abolished by acebutolol suggesting that its ,-adrenoceptor blocking action encompasses peripheral vascular sites. The comparable effect with practolol was a partial inhibition of the diastolic fall.

In studies of eating behavior that have been conducted in humans, the tendency to consume more when given larger portions of food, known as the portion size effect (PSE), is one of the most robust and widely replicated findings. Despite this, the mechanisms that underpin it are still unknown. In particular, it is unclear whether the PSE arises from higher-order social and cognitive processes that are unique to humans or, instead, reflects more fundamental processes that drive feeding, such as conditioned food-seeking. Importantly, studies in rodents and other animals have yet to show convincing evidence of a PSE. In this series of studies, we used several methods to test for a PSE in adult male Sprague Dawley rats. Our approaches included using visually identifiable portions of a palatable food; training on a plate cleaning procedure; providing portion sizes of food pellets that were signaled by auditory and visual food-predictive cues; providing food with amorphous shape properties; and providing standard chow diet portions in home cages. In none of these manipulations did larger portions increase food intake. In summary, our data provide no evidence that a PSE is present in male Sprague Dawley rats, and if it is, it is more nuanced, dependent on experimental procedure, and/or smaller in size than it is in humans. In turn, these findings suggest that the widely-replicated PSE in humans may be more likely to reflect higher-order cognitive and social processes than fundamental conditioned behaviors. Highlights:• Portion size effect (PSE) refers to increased food intake induced by large portions.• Although widely replicated in human feeding studies, it may not exist animals.

In studies of eating behavior that have been conducted in humans, the tendency to consume more when given larger portions of food, known as the portion size effect (PSE), is one of the most robust and widely replicated findings. Despite this, the mechanisms that underpin it are still unknown. In particular, it is unclear whether the PSE arises from higher-order social and cognitive processes that are unique to humans or, instead, reflects more fundamental processes that drive feeding, such as conditioned food-seeking. Importantly, studies in rodents and other animals have yet to show convincing evidence of a PSE. In this series of studies, we used several methods to test for a PSE in adult male Sprague Dawley rats. Our approaches included using visually identifiable portions of a palatable food; training on a plate cleaning procedure; providing portion sizes of food pellets that were signaled by auditory and visual food-predictive cues; providing food with amorphous shape properties;and providing standard chow diet portions in home cages. In none of these manipulations did larger portions increase food intake. In summary, our data provide no evidence that a PSE is present in male Sprague Dawley rats, and if it is, it is more nuanced, dependent on experimental procedure, and/or smaller in size than it is in humans. In turn, these findings suggest that the widely-replicated PSE in humans may be more likely to reflect higher-order cognitive and social processes than fundamental conditioned behaviors. Highlights:• Portion size effect (PSE) refers to increased food intake induced by large portions.• Although widely replicated in human feeding studies, it may not exist animals.• Presence of a PSE in animals would shed light on mechanisms, which are not known.• Here, we find no evidence of PSE in male Sprague Dawley rats under a number of experimental conditions.• This suggests that the human PSE is more likely due to socio-cognitive processes.