Mice lacking δ‐opioid receptors resist the development of diet‐induced obesity

Czyzyk, Traci A.; Romero‐Picó, Amparo; Pintar, John E.; McKinzie, Jaime H.; Tschöp, Matthias H.; Statnick, Michael A.; Nogueiras, Rubén

doi:10.1096/fj.12-208041

Cited by 64 publications

(85 citation statements)

References 51 publications

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“…Twenty-four hours after the liraglutide injection, animals were placed for 6 h in a room with a stable temperature of 4°C as previously described (24). Body temperature was recorded with a rectal probe connected to a digital thermometer, and the interscapular temperature was recorded with an infrared camera.…”

Section: Cold Exposurementioning

confidence: 99%

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

et al. 2014

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GLP-1 receptor (GLP-1R) is widely located throughout the brain, but the precise molecular mechanisms mediating the actions of GLP-1 and its long-acting analogs on adipose tissue as well as the brain areas responsible for these interactions remain largely unknown. We found that central injection of a clinically used GLP-1R agonist, liraglutide, in mice stimulates brown adipose tissue (BAT) thermogenesis and adipocyte browning independent of nutrient intake. The mechanism controlling these actions is located in the hypothalamic ventromedial nucleus (VMH), and the activation of AMPK in this area is sufficient to blunt both central liraglutide-induced thermogenesis and adipocyte browning. The decreased body weight caused by the central injection of liraglutide in other hypothalamic sites was sufficiently explained by the suppression of food intake. In a longitudinal study involving obese type 2 diabetic patients treated for 1 year with GLP-1R agonists, both exenatide and liraglutide increased energy expenditure. Although the results do not exclude the possibility that extrahypothalamic areas are also modulating the effects of GLP-1R agonists, the data indicate that long-acting GLP-1R agonists influence body weight by regulating either food intake or energy expenditure through various hypothalamic sites and that these mechanisms might be clinically relevant.

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Section: Cold Exposurementioning

confidence: 99%

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

et al. 2014

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“…For example, loss of μ, δ opioid and CB1 receptor function prevent obesity mostly by reducing the hedonic value of food. [69][70][71] Furthermore, enhanced μ opioid receptor signalling in the brain is associated with maternal obesity and high-fat feeding before or during pregnancy. 72…”

Section: Box 2 | Brain Circuits Involved In Energy Homeostasismentioning

confidence: 99%

Cognitive and autonomic determinants of energy homeostasis in obesity

Richard

2015

Nat Rev Endocrinol

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Obesity ensues from an imbalance between energy intake and expenditure that results from gene-environment interactions, which favour a positive energy balance. A society that promotes unhealthy food and encourages sedentary lifestyle (that is, an obesogenic environment) has become a major contributory factor in excess fat deposition in individuals predisposed to obesity. Energy homeostasis relies upon control of energy intake as well as expenditure, which is in part determined by the themogenesis of brown adipose tissue and mediated by the sympathetic nervous system. Several areas of the brain that constitute cognitive and autonomic brain systems, which in turn form networks involved in the control of appetite and thermogenesis, also contribute to energy homeostasis. These networks include the dopamine mesolimbic circuit, as well as the opioid, endocannabinoid and melanocortin systems. The activity of these networks is modulated by peripheral factors such as hormones derived from adipose tissue and the gut, which access the brain via the circulation and neuronal signalling pathways to inform the central nervous system about energy balance and nutritional status. In this Review, I focus on the determinants of energy homeostasis that have emerged as prominent factors relevant to obesity.

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“…Human and animal studies suggest that adiposity-induced leptin increase and subsequent leptin resistance would affect these transmitters, causing or worsening asthma symptoms. This relates both to orexigenic neuropeptides such as neuropeptide Y (114)(115)(116)(117)(118)(119)(120) , endocannabinoids (121,122) , endogenous opioids (123)(124)(125)(126) ; and anorexigenic neuropeptides such as tachykinins and its most studied members substance P (127)(128)(129)(130)(131)(132) , α-melanocyte-stimulating hormone (133)(134)(135) , corticotropin-releasing factor (136)(137)(138)(139)(140)(141) and serotonin (142)(143)(144)(145)(146)(147)(148)(149)(150) . Altogether, it suggests that these peptides can modulate asthmatic inflammation among obese patients.…”

Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.

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Mice lacking δ‐opioid receptors resist the development of diet‐induced obesity

Cited by 64 publications

References 51 publications

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

Cognitive and autonomic determinants of energy homeostasis in obesity

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

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