scholarly journals The role of thermoregulatory thermogenesis in the development of obesity in genetically-obese (ob/ob) mice pair-fed with lean siblings

1979 ◽  
Vol 42 (3) ◽  
pp. 377-385 ◽  
Author(s):  
P. L. Thurlby ◽  
P. Trayhurn

1. In order to quantitatively assess the energetic significance of reduced thermoregulatory thermogenesis in the accumulation of excess body fat in genetically-obese (ob/ob) mice experiments have been conducted at four environmental temperatures (17, 23, 28 and 33°) in which young growing obese animals were pair-fed for 10 d to the ad lib. intake of lean siblings.2. The food intake of the lean mice increased with decreasing environmental temperature: at 17° the intake was 86% higher than that at 33°.3. The estimated gain in carcass energy of lean mice rose with increasing temperature, from 82 kJ at 17° to 150 kJ at 33°. The energy gain of the pair-fed obese mice was higher than that of the lean at all temperatures but showed a slight decrease with increasing temperature, from 231 kJ at 17° to 191 kJ at 33°.4. Environmental temperature affected the ‘excess’ energy gain of the obese mice. At 17° the obese mice deposited 182% more energy than the lean but this difference decreased progressively with increasing temperature to 127, 62 and 27% more energy at 23, 28 and 33° respectively.5. At all environmental temperatures the pair-fed obese mice deposited considerably less protein than their lean controls. The deposition ranged from 32% (at 17°) to 56% (at 28°) of that of the lean mice.6. It is concluded that environmental temperature plays a major role in determining the excess energy gain of ob/ob mice receiving the same amount of food as lean controls, and that the low energy expenditure and consequent high metabolic efficiency of this mutant is due primarily to reduced thermoregulatory thermogenesis.

2020 ◽  
Vol 9 ◽  
Author(s):  
Paul Trayhurn ◽  
Jonathan R. S. Arch

Abstract Rodents with mutations in the leptin, or leptin receptor, genes have been extensively used to investigate the regulation of energy balance and the factors that underlie the development of obesity. The excess energy gain of these mutants has long been considered as being due in part to increased metabolic efficiency, consequent to reduced energy expenditure, but this view has recently been challenged. We argue, particularly though not exclusively, from data on ob/ob mice, that three lines of evidence support the proposition that reduced expenditure is important in the aetiology of obesity in leptin pathway mutants (irrespective of the genetic background): (i) milk intake is similar in suckling ob/ob and +/? mice; (ii) ob/ob mice deposit excess energy when pair-fed to the ad libitum food intake of lean siblings; (iii) in several studies mutant mice have been shown to exhibit a lower RMR ‘per animal’ at temperatures below thermoneutrality. When metabolic rate is expressed ‘per unit body weight’ (inappropriately, because of body composition differences), then it is invariably lower in the obese than the lean. It is important to differentiate the causes from the consequences of obesity. Hyperphagic, mature obese animals weighing 2–3 times their lean siblings may well have higher expenditure ‘per animal’, reflecting the costs of being larger and of enhanced obligatory diet-induced thermogenesis resulting from the increased food intake. This cannot, however, be used to inform the aetiology of their obesity.


1986 ◽  
Vol 251 (6) ◽  
pp. R1118-R1125
Author(s):  
T. J. Bartness ◽  
C. J. Billington ◽  
A. S. Levine ◽  
J. E. Morley ◽  
N. E. Rowland ◽  
...  

The role of insulin in metabolic efficiency (ME, i.e., efficiency of body wt gain) was examined under conditions of maximal energy expenditure in control and diabetic rats. Long-lasting insulin was administered using a protocol that did not affect food intake and increased ME in both groups. Half the animals were injected chronically with norepinephrine (NE). NE alone in controls decreased body weight and ME and increased brown adipose tissue (BAT) growth, thermogenic potential [cytochrome c oxidase activity (COA)], and lipoprotein lipases (LPL) activity; however, in diabetics, body weight, ME, and food intake all decreased and only BAT LPL activity and DNA content increased. The combination of NE and insulin increased BAT protein and COA in diabetics; in controls, all BAT measures were further increased and ME was intermediate to that of either treatment alone. Cold exposure decreased body weight and ME, increased food intake and qualitatively produced similar increases in BAT growth, COA, and LPL activity in both controls and diabetics. In diabetics, combined cold exposure and insulin did not affect the increase in BAT growth or LPL activity resulting from either treatment alone, but in controls this combination decreased BAT growth and COA. It is concluded that, even under conditions of maximal energy expenditure, both extremes of basal insulin status result in decreased BAT growth and thermogenic potential, but have opposite effects on ME.


The young rat adjusts its food intake so precisely to its energy needs that its fat stores remain almost constant. Considerable variation in food intake is brought about in response to change in heat loss to the environment, or in loss of food through the mammary gland in lactation, without appreciable change of weight. Hypothalamic damage permits excessive intake and causes obesity. The degree of obesity and in general its rate of development, is a function of the degree of dam age to the region of the tuber cinereum , and is independent of changes of intake with environmental temperature. It is suggested that the hypothalamic satiety mechanism is concerned only in the prevention of an overall surplus of energy intake over expenditure, which would cause the deposition of fat in the depots. The simplest way in which this lipostasis could be achieved is b y sensitivity to the concentration of circulating metabolites. There is no disturbance of temperature regulation or acclimatization to changed environmental temperature in obese rats. These findings do not support the suggestion made by Brobeck (1946) that food intake is controlled as part of the normal regulation of body temperature by a thermosensitive hypothalamic centre. The maximum daily in take of food during hyperphagia appears to be determined by some limiting factor additional to the hypothalamic mechanism. A similar factor appears to operate in lactation. Reasons are advanced for regarding this as the limiting rate at which absorbed foodstuffs can be removed from the circulation, that is as some aspect of the synthesis or transport of fat.


1960 ◽  
Vol 55 (3) ◽  
pp. 359-364 ◽  
Author(s):  
A. Rogerson

1. A relatively inexpensive closed-circuit respiration chamber for cattle is described.2. Experiments with two steers are reported in which heat production and energy retention data were measured at different levels of food intake and at different environmental temperatures.3. The energy lost in faeces increased with improving plane of nutrition but was not significantly affected by the environmental temperature. Urine energy losses fell with increasing environmental temperature at low planes of nutrition. Methane losses increased with improving nutritional plane but were reduced by high environmental temperatures at high levels of food intake.4. The heat production of fasting animals, or animals on low planes of nutrition was not influenced by the environmental temperature in the range 20–40° C. On higher planes of nutrition an increasing environmental temperature increased the animals' heat production.5. The major factor determining energy retention in different environments is the heat production of the animal. Net energy values consequently vary with temperature.


1994 ◽  
Vol 266 (1) ◽  
pp. R164-R168 ◽  
Author(s):  
J. E. Morley ◽  
J. F. Flood

Recent studies have suggested a role for nitric oxide (NO) in the regulation of food intake. The present studies were undertaken to examine the effects of the administration of a nitric oxide synthetase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on food intake and weight loss. Two genetically obese mice, the ob/ob and db/db strains, and their lean heterozygote littermate controls, ob/c and db/c, served as subjects. In the first experiment, we demonstrated that L-NAME (100 micrograms/kg) given twice over a feeding period of 7 h/day produced a small but significant weight loss in ob/ob mice but not in their lean-genotype controls (P < 0.05). In the second experiment, a higher dose of L-NAME (100 mg/kg), given twice daily, produced a marked effect on body weight, with the ob/ob mice losing approximately 10% of their body weight in 9 days. The ob/c mice showed a lesser decrease in body weight. Food intake was decreased on all 9 days in the ob/ob mice (P < 0.01). A small decrease in body weight and food intake was seen in db/db and db/c mice receiving L-NAME. These studies provide further evidence for a role of nitric oxide in the modulation of food intake and weight gain.


1994 ◽  
Vol 267 (1) ◽  
pp. R178-R184 ◽  
Author(s):  
J. E. Morley ◽  
J. F. Flood ◽  
M. Horowitz ◽  
P. M. Morley ◽  
M. J. Walter

Amylin has been demonstrated to produce anorexia in rodents. Its mechanism of action is unknown. We have studied the effect of amylin on food intake in mice in a variety of paradigms to determine whether it inhibits food intake by a peripheral mechanism of action. In addition, we determined its effect in genetically obese mice models and whether its effects differed in aged mice. Cholecystokinin is the prototypic satiety agent. The effects of amylin on reducing food intake were not attenuated by the cholecystokinin antagonist L-364718, suggesting that it does not produce its effect through the release of cholecystokinin. A number of gastrointestinal peptides produce anorexia by stimulating ascending vagal fibers. For this reason, we studied the effect of truncal vagotomy on the suppression of feeding induced by amylin. Vagotomy did not prevent amylin from inhibiting food intake. Amylin was equally effective at reducing food intake in genetically obese (ob/ob) and lean (ob/c) mice and in diabetic (db/db) and lean (db/c) mice. Amylin effectively suppressed food intake in mice over the age of 4-22 mo. These studies further support the role of the pancreatic hormone amylin as a peripherally acting satiety agent.


2019 ◽  
pp. 155-161 ◽  
Author(s):  
Ivan Beltran

Environmental temperature has fitness consequences on ectotherm development, ecology and behaviour. Amphibians are especially vulnerable because thermoregulation often trades with appropriate water balance. Although substantial research has evaluated the effect of temperature in amphibian locomotion and physiological limits, there is little information about amphibians living under extreme temperature conditions. Leptodactylus lithonaetes is a frog allegedly specialised to forage and breed on dark granitic outcrops and associated puddles, which reach environmental temperatures well above 40 ˚C. Adults can select thermally favourable microhabitats during the day while tadpoles are constrained to rock puddles and associated temperature fluctuations; we thus established microhabitat temperatures and tested whether the critical thermal maximum (CTmax) of L. lithonaetes is higher in tadpoles compared to adults. In addition, we evaluated the effect of water temperature on locomotor performance of tadpoles. Contrary to our expectations, puddle temperatures were comparable and even lower than those temperatures measured in the microhabitats used by adults in the daytime. Nonetheless, the CTmax was 42.3 ˚C for tadpoles and 39.7 ˚C for adults. Regarding locomotor performance, maximum speed and maximum distance travelled by tadpoles peaked around 34 ˚C, approximately 1 ˚C below the maximum puddle temperatures registered in the puddles. In conclusion, L. lithonaetes tadpoles have a higher CTmax compared to adults, suggesting a longer exposure to extreme temperatures that lead to maintain their physiological performance at high temperatures. We suggest that these conditions are adaptations to face the strong selection forces driven by this granitic habitat.


Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1158
Author(s):  
Lizeth Cifuentes ◽  
Michael Camilleri ◽  
Andres Acosta

Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.


2021 ◽  
Author(s):  
Aline GIROUX ◽  
Zaida ORTEGA ◽  
Alessandra BERTASSONI ◽  
Arnaud Léonard Jean DESBIEZ ◽  
Danilo KLUYBER ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document