Modulation of central leptin sensitivity and energy balance in a rat model of diet‐induced obesity

Fam, Barbara C; Morris, Margaret J.; Hansen, Michelle; Kebede, Melkam A.; Andrikopoulos, Sofianos; Proietto, Joseph; Thorburn, Anne W.

doi:10.1111/j.1463-1326.2006.00653.x

Cited by 65 publications

(59 citation statements)

References 66 publications

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“…Our findings showing increased food intake despite changes in hormones that promote satiety/reduce hunger are consistent with findings from studies of clock mutant mice (34) and sleeprestricted ad libitum fed humans (21). The controlled CTRC study limited the duration of sleep loss and thus it is possible that given a longer time course of overeating, participants would have responded to changes in satiety and hunger hormones (35). Changes in other hormones not examined may also promote food intake during sleep loss (e.g., cholecystokinin, glucagon-like peptide-1).…”

Section: Energy Expenditure and Energy Intake During Sleep Loss Andsupporting

confidence: 79%

Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain

Markwald

Melanson

Smith

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

656

592

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Insufficient sleep is associated with obesity, yet little is known about how repeated nights of insufficient sleep influence energy expenditure and balance. We studied 16 adults in a 14-to 15-d-long inpatient study and quantified effects of 5 d of insufficient sleep, equivalent to a work week, on energy expenditure and energy intake compared with adequate sleep. We found that insufficient sleep increased total daily energy expenditure by ∼5%; however, energy intake-especially at night after dinner-was in excess of energy needed to maintain energy balance. Insufficient sleep led to 0.82 ± 0.47 kg (±SD) weight gain despite changes in hunger and satiety hormones ghrelin and leptin, and peptide YY, which signaled excess energy stores. Insufficient sleep delayed circadian melatonin phase and also led to an earlier circadian phase of wake time. Sex differences showed women, not men, maintained weight during adequate sleep, whereas insufficient sleep reduced dietary restraint and led to weight gain in women. Our findings suggest that increased food intake during insufficient sleep is a physiological adaptation to provide energy needed to sustain additional wakefulness; yet when food is easily accessible, intake surpasses that needed. We also found that transitioning from an insufficient to adequate/recovery sleep schedule decreased energy intake, especially of fats and carbohydrates, and led to −0.03 ± 0.50 kg weight loss. These findings provide evidence that sleep plays a key role in energy metabolism. Importantly, they demonstrate physiological and behavioral mechanisms by which insufficient sleep may contribute to overweight and obesity.calorimetry | misalignment | dysregulated eating | deprivation | restriction M ore than 1.4 billion adults, 150 million school-aged children, and 43 million preschool children are estimated to be overweight or obese worldwide (1-3), substantially raising risk for cardiovascular diseases (4) hyperlipidemia (5), diabetes (5, 6), osteoarthritis (6), sleep apnea (7), depression (8), and cancer (9). Excessive food consumption and inadequate physical activity are primary factors contributing to the obesity epidemic. When daily energy intake is in excess of energy expenditure (EE) a state of positive energy balance occurs. Over weeks, months, or years, a small cumulative impact of sustained positive energy balance results in weight gain and obesity (10). Alongside the rise in obesity there has been a decline in the number of individuals who report obtaining the recommended 7-9 h of sleep, with many obtaining less than 6 h per night (11). Insufficient sleep is a risk factor of weight gain and obesity (11-13), yet how insufficient sleep contributes to this risk is unclear. Sleep influences energy metabolism (14, 15), and one function of sleep is to conserve energy (16). Proposed mechanisms that associate insufficient sleep and higher body mass index (BMI) include changes in satiety and hunger hormones altering food intake and changes in EE (17). Insufficient sleep is associated with decreases...

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Section: Energy Expenditure and Energy Intake During Sleep Loss Andsupporting

confidence: 79%

Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain

Markwald

Melanson

Smith

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

656

592

View full text Add to dashboard Cite

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“…A more recent study showed that adult male SpragueDawley rats fed a high-fat diet (60 % of energy) for 2 weeks were hypersensitive to the food intake-lowering effect of ICV administration of leptin (3 mg); however, after 5 weeks on the high-fat diet, rats became insensitive to this effect of injected leptin (185) . Another study in weanling C57BL/6J mice led to similar conclusions (186) .…”

Section: Hormonesmentioning

confidence: 99%

High-fat diet-induced obesity in animal models

2010

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Epidemiological studies have shown a positive relationship between dietary fat intake and obesity. Since rats and mice show a similar relationship, they are considered an appropriate model for studying dietary obesity. The present paper describes the history of using high-fat diets to induce obesity in animals, aims to clarify the consequences of changing the amount and type of dietary fats on weight gain, body composition and adipose tissue cellularity, and explores the contribution of genetics and sex, as well as the biochemical basis and the roles of hormones such as leptin, insulin and ghrelin in animal models of dietary obesity. The major factors that contribute to dietary obesity -hyperphagia, energy density and post-ingestive effects of the dietary fat -are discussed. Other factors that affect dietary obesity including feeding rhythmicity, social factors and stress are highlighted. Finally, we comment on the reversibility of high-fat diet-induced obesity.

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“…The metabolic effects of leptin in relation to body weight and energy balance have been well-described, although the mechanisms underlying the relative central resistance to leptin in obesity remain unclear (Fam et al 2007;Wilsey et al 2003;Friedman and Halaas, 1998). In addition, it has recently become apparent that leptin may be an important endocrine factor in driving the promotion of several obesity-related cancers.…”

Section: Introductionmentioning

confidence: 99%

Globular adiponectin, acting via adiponectin receptor-1, inhibits leptin-stimulated oesophageal adenocarcinoma cell proliferation

Ogunwobi

Beales

2008

Molecular and Cellular Endocrinology

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Obesity increases the risk of developing several cancers including oesophageal adenocarcinoma (OAC). Obesity is characterized by hyperleptinaemia and hypoadiponectinaemia: we have hypothesized that these hormonal factors may contribute to the progression of OAC. We have examined the effects of leptin and adiponectin on proliferation of OAC cells. Leptin stimulated proliferation in 4 different OAC lines (OE33, OE19, BIC-1 and FLO) and this was inhibited by globular but not full length adiponectin. All 4 OAC lines expressed both adiponectin-receptor isoforms (AdipoR1 and AdipoR2).

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Modulation of central leptin sensitivity and energy balance in a rat model of diet‐induced obesity

Cited by 65 publications

References 66 publications

Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain

Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain

High-fat diet-induced obesity in animal models

Globular adiponectin, acting via adiponectin receptor-1, inhibits leptin-stimulated oesophageal adenocarcinoma cell proliferation

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