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Article ; Online: Activation of the central melanocortin system in rats persistently reduces body and fat mass independently of caloric reduction.

Côté, Isabelle / Green, Sara M / Morgan, Drake / Carter, Christy S / Tümer, Nihal / Scarpace, Philip J

Canadian journal of physiology and pharmacology

2017 Volume 96, Issue 3, Page(s) 308–312

Abstract: Recent evidence indicate that melanotan II (MTII) reduces body mass independently of caloric reduction. Because MTII induces a transient hypophagia, caloric reduction is still considered a primary mechanism for MTII-mediated body mass loss. To examine ... ...

Abstract	Recent evidence indicate that melanotan II (MTII) reduces body mass independently of caloric reduction. Because MTII induces a transient hypophagia, caloric reduction is still considered a primary mechanism for MTII-mediated body mass loss. To examine the contribution of caloric reduction to long-term body mass loss in response to MTII, we centrally infused MTII or vehicle in ad libitum fed (MTII and Control) animals in comparison with a group of animals that were pair-fed (PF) to the MTII group. Food intake and body mass were recorded daily, and body composition was assessed biweekly. The present study demonstrates that central MTII-mediated body mass loss is only partially mediated by caloric restriction, and the long-term body mass loss is independent of the initial hypophagia. More importantly, central MTII administration induced a rapid but sustained fat mass loss, independently of caloric reduction. MTII-treated animals preserved their lean/fat mass ratio throughout the study, whereas PF animals underwent a transient reduction of lean/fat mass ratio that was only normalized when food intake returned to Control level. In summary, it can be concluded that activation of the central melanocortin system in rats persistently reduces body and fat mass independently of caloric reduction.
MeSH term(s)	Adipose Tissue/cytology ; Adipose Tissue/drug effects ; Animals ; Body Weight/drug effects ; Caloric Restriction ; Eating/drug effects ; Male ; Melanocortins/metabolism ; Peptides, Cyclic/pharmacology ; Rats ; alpha-MSH/analogs & derivatives ; alpha-MSH/pharmacology
Chemical Substances	Melanocortins ; Peptides, Cyclic ; melanotan-II (121062-08-6) ; alpha-MSH (581-05-5)
Language	English
Publishing date	2017-11-13
Publishing country	Canada
Document type	Journal Article
ZDB-ID	127527-6
ISSN	1205-7541 ; 0008-4212
ISSN (online)	1205-7541
ISSN	0008-4212
DOI	10.1139/cjpp-2017-0440
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Article ; Online: The soluble leptin receptor neutralizes leptin-mediated STAT3 signalling and anorexic responses in vivo.

Zhang, Jiejin / Scarpace, Philip J

British journal of pharmacology

2009 Volume 158, Issue 2, Page(s) 475–482

Abstract: Background and purpose: The soluble leptin receptor (SLR) is the major, circulating, leptin-binding protein and, in vitro, the SLR inhibits leptin-binding to cell surface receptors. Here we assessed the effects of the SLR on physiological responses to ... ...

Abstract	Background and purpose: The soluble leptin receptor (SLR) is the major, circulating, leptin-binding protein and, in vitro, the SLR inhibits leptin-binding to cell surface receptors. Here we assessed the effects of the SLR on physiological responses to leptin, in vivo. Experimental approach: SLR and leptin were given as a single injection (intracerebroventricularly, i.c.v.) or by central (i.c.v.) and peripheral (s.c.) infusion to normal adult F344XBN rats. Phosphorylation of hypothalamic STAT3 (Western blot), food intake and body weight, and the thermogenic response in brown adipose tissue (BAT) were measured. Key results: Acute central co-administration of SLR (13.5 microg) and leptin (90 ng) blocked the threefold increase in hypothalamic STAT3 phosphorylation induced by leptin alone, 1 h after the injections. Peripheral leptin infusion (0.1 mg day(-1) for 7 days; s.c.) induced a significant reduction in food intake and body weight, which were partially blocked with a simultaneous central infusion of SLR (4.3 microg day(-1); i.c.v.). In a second experiment, SLR central infusion alone (5.5 microg day(-1)) increased food intake and body weight, suggesting that the SLR was able to neutralize endogenous leptin in the brain. This dose of SLR, infused together with a lower dose of peripheral leptin (0.05 mg day(-1)), abolished the thermogenic response in BAT, but the anorexic responses and weight reduction were only partially attenuated. Conclusions: These results provide direct evidence that the SLR neutralizes leptin, endogenous or exogenous, in vivo. By neutralizing leptin, the SLR may play a regulatory role in energy homeostasis.
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Animals ; Blotting, Western ; Body Weight/physiology ; Dose-Response Relationship, Drug ; Eating/physiology ; Hypothalamus/metabolism ; Leptin/administration & dosage ; Leptin/metabolism ; Male ; Phosphorylation/physiology ; Rats ; Rats, Inbred BN ; Rats, Inbred F344 ; Receptors, Leptin/administration & dosage ; Receptors, Leptin/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction/physiology
Chemical Substances	Leptin ; Receptors, Leptin ; STAT3 Transcription Factor ; Stat3 protein, rat
Language	English
Publishing date	2009-05-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/j.1476-5381.2009.00246.x
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Article: Leptin resistance: a prediposing factor for diet-induced obesity.

Scarpace, Philip J / Zhang, Yi

American journal of physiology. Regulatory, integrative and comparative physiology

2008 Volume 296, Issue 3, Page(s) R493–500

Abstract: Obesity is a resilient and complex chronic disease. One potential causative factor in the obesity syndrome is leptin resistance. Leptin behaves as a potent anorexic and energy-enhancing hormone in most young or lean animals, but its effects are ... ...

Abstract	Obesity is a resilient and complex chronic disease. One potential causative factor in the obesity syndrome is leptin resistance. Leptin behaves as a potent anorexic and energy-enhancing hormone in most young or lean animals, but its effects are diminished or lacking in the obese state associated with a normal genetic background. Emerging evidence suggests that leptin resistance predisposes the animal to exacerbated diet-induced obesity (DIO). Elevation of central leptin in young, lean rats induces a leptin resistance that precludes obesity on a chow diet but accelerates high-fat (HF)-induced obesity. Similarly, chronic dietary fructose consumption evokes a leptin resistance that causes obesity only upon HF exposure. Inherent central leptin insensitivity also contributes to dietary weight gain in certain obesity-prone rats. Conversely, aged, leptin-resistant animals are obese with continuous chow feeding and demonstrate aggravated obesity when challenged with an HF diet. Additionally, a submaximal central blockade with a leptin antagonist leads to obesity on both chow and HF diets, as is the case in rodents with leptin receptor deficiency of genetic origin. Despite the differences in the incidence of obesity on a chow diet, all of these forms of leptin resistance predispose rodents to aggravated HF-mediated obesity. Moreover, once leptin resistance takes hold, it aggravates DIO, and the leptin resistance and obesity compound one another, promoting a vicious cycle of escalating weight gain.
MeSH term(s)	Aging/physiology ; Animals ; Body Composition/physiology ; Diet ; Humans ; Leptin/antagonists & inhibitors ; Leptin/physiology ; Obesity/physiopathology
Chemical Substances	Leptin
Language	English
Publishing date	2008-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.90669.2008
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Article ; Online: Protective effects of resveratrol on aging-induced cognitive impairment in rats.

Gocmez, Semil Selcen / Gacar, Nejat / Utkan, Tijen / Gacar, Gulcin / Scarpace, Philip J / Tumer, Nihal

Neurobiology of learning and memory

2016 Volume 131, Page(s) 131–136

Abstract: Resveratrol, a polyphenol phytoalexine, has been shown to play a neuroprotective role in the neurodegenerative process in Alzheimer's disease (AD) and improve memory function in dementia. However, the in vivo effect of resveratrol in normal aging models ... ...

Abstract	Resveratrol, a polyphenol phytoalexine, has been shown to play a neuroprotective role in the neurodegenerative process in Alzheimer's disease (AD) and improve memory function in dementia. However, the in vivo effect of resveratrol in normal aging models of learning and memory has not yet been evaluated. Therefore, the present neurobehavioral study was undertaken to evaluate the effect of resveratrol on cognitive impairment induced by aging in passive avoidance and Morris water maze (MWM) tests. Male Wistar albino rats were divided into four groups: young control (4month), young resveratrol (4month+RESV), old control (24month) and old resveratrol (24month+RESV). Resveratrol (50mg/kg/day) was given to the 4month+RESV and 24month+RESV groups orally for 12weeks. There was no significant difference between the groups for the first day of latency, while in aged rats, the second day of latency was significantly shortened compared to the young group in the passive avoidance test (p<0.05). Additionally, in the MWM test, the results showed a decrease in the time spent in the escape platform's quadrant in the probe test in aged rats (p<0.05). The administration of resveratrol at 50mg/kg/day increased the retention scores in the passive avoidance test and the time spent in the escape platform's quadrant in the MWM task (p<0.05). Furthermore resveratrol attenuated the protein levels of TNFα and IL1β in the 24-month group. These findings indicate that aging impairs emotional and spatial learning-memory and resveratrol reverses the effect of age-related learning and memory impairment. The results of this study suggest that resveratrol is effective in preventing cognitive deficit in aged rats by inhibiting the production of inflammatory cytokines.
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ZDB-ID	1223366-3
ISSN	1095-9564 ; 1074-7427
ISSN (online)	1095-9564
ISSN	1074-7427
DOI	10.1016/j.nlm.2016.03.022
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Zs.B 2339: Show issues

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Article ; Online: ACE2 activator diminazene aceturate reduces adiposity but preserves lean mass in young and old rats.

Bruce, Erin B / Sakarya, Yasemin / Kirichenko, Nataliya / Toklu, Hale Z / Sumners, Colin / Morgan, Drake / Tümer, Nihal / Scarpace, Philip J / Carter, Christy S

Experimental gerontology

2018 Volume 111, Page(s) 133–140

Abstract: The obesity epidemic is multi-generational and is particularly debilitating in the aging population, necessitating the use of pharmaceutical interventions. Recent evidence suggests that increasing the activity of the angiotensin converting enzyme-2 [ACE2] ...

Abstract	The obesity epidemic is multi-generational and is particularly debilitating in the aging population, necessitating the use of pharmaceutical interventions. Recent evidence suggests that increasing the activity of the angiotensin converting enzyme-2 [ACE2]/angiotensin-(1-7)[Ang-(1-7)]/Mas receptor (MasR) axis in obese animal models leads to significant reductions in body weight. It was hypothesized that activation of ACE2 via diminazene aceturate (DIZE) will significantly reduce body weight of rats fed a high fat diet. Young and old (4 and 23 months, respectively) male Fisher 344 × Brown Norway rats were fed 60% high fat diet for one week, and subsequently given either 15 mg/kg/day DIZE s.c. or vehicle for three weeks. DIZE treatment resulted in a significant reduction of food intake and body weight in both young and old animals. However, that decrease was so dramatic in the older animals that they all nearly stopped eating. Interestingly, the TD-NMR assessments revealed that the weight-loss was primarily a result of decreased body fat percentage, with a relative preservation of lean mass. Tissue weights confirm the significant loss of white adipose tissue (WAT), with no change in muscle weights. Gene expression and serum ACE2 activity analyses implied that increased activation of the ACE2/Ang-(1-7)/MasR axis plays a role in reducing fat mass. Collectively, our results suggest that DIZE may be a useful tool in the study of obesity; however, caution is recommended when using this compound in older animals due to severe anorectic effects, although there is a mechanism by which muscle is preserved.
MeSH term(s)	Adiposity/drug effects ; Age Factors ; Angiotensin I/genetics ; Angiotensin I/metabolism ; Animals ; Diminazene/analogs & derivatives ; Diminazene/pharmacology ; Disease Models, Animal ; Gene Expression ; Male ; Obesity/metabolism ; Peptide Fragments/genetics ; Peptide Fragments/metabolism ; Peptidyl-Dipeptidase A/blood ; Peptidyl-Dipeptidase A/genetics ; Peptidyl-Dipeptidase A/metabolism ; Rats ; Rats, Inbred F344 ; Renin-Angiotensin System/drug effects
Chemical Substances	Peptide Fragments ; Angiotensin I (9041-90-1) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; angiotensin converting enzyme 2 (EC 3.4.17.-) ; angiotensin I (1-7) (IJ3FUK8MOF) ; diminazene aceturate (JI8SAD85NO) ; Diminazene (Y5G36EEA5Z)
Language	English
Publishing date	2018-07-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	390992-x
ISSN	1873-6815 ; 0531-5565
ISSN (online)	1873-6815
ISSN	0531-5565
DOI	10.1016/j.exger.2018.07.008
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Article ; Online: Limiting feeding to the active phase reduces blood pressure without the necessity of caloric reduction or fat mass loss.

Cote, Isabelle / Toklu, Hale Z / Green, Sara M / Morgan, Drake / Carter, Christy S / Tümer, Nihal / Scarpace, Philip J

American journal of physiology. Regulatory, integrative and comparative physiology

2018 Volume 315, Issue 4, Page(s) R751–R758

Abstract: Reducing body weight has been shown to lower blood pressure in obesity-related hypertension. However, success of those lifestyle interventions is limited due to poor long-term compliance. Emerging evidence indicates that feeding schedule plays a role on ... ...

Abstract	Reducing body weight has been shown to lower blood pressure in obesity-related hypertension. However, success of those lifestyle interventions is limited due to poor long-term compliance. Emerging evidence indicates that feeding schedule plays a role on the regulation of blood pressure. With two studies, we examined the role of feeding schedule on energy homeostasis and blood pressure. In study 1, rats were fed a high-fat diet (HFD) ad libitum for 24 h (Control) or for 12 h during the dark phase (time-restricted feeding, TRF). In study 2, rats fed a HFD were administered a long-acting α-MSH analog at either light onset [melanotan II (MTII) light] or dark onset (MTII dark) or saline (Control). MTII light animals ate most of their calories during the active phase, similar to the TRF group. In study 1, Control and TRF rats consumed the same amount of food and gained the same amount of weight and fat mass. Interestingly, systolic and mean arterial pressure (MAP) was lower in the TRF group. In study 2, food intake was significantly lower in both MTII groups relative to Control. Although timing of injection affected light versus dark phase food consumption, neither body weight nor fat mass differed between MTII groups. Consistent with study 1, rats consuming their calories during the active phase displayed lower MAP. These data indicate that limiting feeding to the active phase reduces blood pressure without the necessity of reducing calories or fat mass, which could be relevant to obesity-related hypertension.
MeSH term(s)	Activity Cycles ; Adiposity/drug effects ; Animals ; Arterial Pressure/drug effects ; Diet, High-Fat ; Disease Models, Animal ; Energy Intake ; Energy Metabolism/drug effects ; Fasting ; Feeding Behavior/drug effects ; Hypertension/diet therapy ; Hypertension/metabolism ; Hypertension/physiopathology ; Male ; Obesity/diet therapy ; Obesity/metabolism ; Obesity/physiopathology ; Peptides, Cyclic/administration & dosage ; Photoperiod ; Rats, Inbred BN ; Rats, Inbred F344 ; Time Factors ; alpha-MSH/administration & dosage ; alpha-MSH/analogs & derivatives
Chemical Substances	Peptides, Cyclic ; melanotan-II (121062-08-6) ; alpha-MSH (581-05-5)
Language	English
Publishing date	2018-07-19
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00076.2018
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Article: Elevated leptin: consequence or cause of obesity?

Scarpace, Philip J / Zhang, Yi

Frontiers in bioscience : a journal and virtual library

2007 Volume 12, Page(s) 3531–3544

Abstract: Leptin is an adipocyte-derived, satiety-regulating hormone that acts within the hypothalamus and other brain sites. Obese humans and animals are largely resistant to central actions of leptin. Rising leptin levels associated with progressing obesity are ... ...

Abstract	Leptin is an adipocyte-derived, satiety-regulating hormone that acts within the hypothalamus and other brain sites. Obese humans and animals are largely resistant to central actions of leptin. Rising leptin levels associated with progressing obesity are generally regarded as simply a consequence rather than a causative factor in the leptin resistance and obesity. Several lines of evidence suggest otherwise. Chronic overexpression of central leptin induces a leptin resistance that mimics many of the characteristics associated with diet-induced or adult-onset obesity including reduced leptin receptors, diminished signaling, and impaired responsiveness to exogenous leptin. Moreover, these animals have increased susceptibility to diet-induced obesity. New data with a leptin antagonist demonstrate that blockade of leptin receptors also exaggerates diet-induced obesity. These findings suggest an important role for elevated leptin in the development of leptin resistance and obesity, especially in today's society with an overabundance of readily available high caloric food. Once leptin resistance takes hold, each subsequent exposure to high-density food faces diminished counter-regulatory responses, leading to exacerbated weight gain.
MeSH term(s)	Adult ; Diet ; Drug Resistance ; Humans ; Leptin/blood ; Obesity/blood ; Obesity/physiopathology ; Signal Transduction
Chemical Substances	Leptin
Language	English
Publishing date	2007-05-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2141320-4
ISSN	1093-9946
ISSN	1093-9946
DOI	10.2741/2332
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Zs.A 5867: Show issues

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Article: Circumventing central leptin resistance: lessons from central leptin and POMC gene delivery.

Zhang, Yi / Scarpace, Philip J

Peptides

2006 Volume 27, Issue 2, Page(s) 350–364

Abstract: We identified that leptin resistance in aged-obese rats has both peripheral and central components. The central resistance is characterized by diminished hypothalamic leptin receptors and impaired leptin signal transduction. We developed a new model of ... ...

Abstract	We identified that leptin resistance in aged-obese rats has both peripheral and central components. The central resistance is characterized by diminished hypothalamic leptin receptors and impaired leptin signal transduction. We developed a new model of leptin-induced leptin resistance in which application of the central leptin gene delivery produces unabated hypothalamic leptin over-expression. The chronic central elevation of leptin precipitates leptin resistance in young animals devoid of obesity and exacerbates it in mature or aged animals with obesity. Despite leptin resistance, our aged obese, DIO, and leptin-induced leptin resistant rats were fully responsive to central pharmacological melanocortin activation. We propose that the central leptin resistance resides between leptin receptor and melanocortin receptor activation. Our central POMC gene therapy overcame leptin resistance, producing weight and fat loss and improved insulin sensitivity in obese Zucker and aged rats. This success highlights the central melanocortin system as a useful drug target for combating obesity.
MeSH term(s)	Adiposity/drug effects ; Animals ; Drug Resistance/genetics ; Drug Resistance/physiology ; Energy Metabolism/drug effects ; Gene Transfer Techniques ; Leptin/blood ; Leptin/genetics ; Leptin/pharmacology ; Melanocyte-Stimulating Hormones/metabolism ; Models, Animal ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/metabolism ; Pro-Opiomelanocortin/pharmacology ; Rats ; STAT3 Transcription Factor/metabolism
Chemical Substances	Leptin ; STAT3 Transcription Factor ; Pro-Opiomelanocortin (66796-54-1) ; Melanocyte-Stimulating Hormones (9002-79-3)
Language	English
Publishing date	2006-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2005.01.024
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Zs.A 1649: Show issues

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Article: The role of leptin in leptin resistance and obesity.

Zhang, Yi / Scarpace, Philip J

Physiology & behavior

2006 Volume 88, Issue 3, Page(s) 249–256

Abstract: Although the presence of hyperleptinemia with leptin resistance and obesity has long been recognized, a causal role of elevated leptin in these biological states remains unclear. This article summarizes some recent work from our laboratory supporting the ...

Abstract	Although the presence of hyperleptinemia with leptin resistance and obesity has long been recognized, a causal role of elevated leptin in these biological states remains unclear. This article summarizes some recent work from our laboratory supporting the concept that leptin, in and of itself, promotes leptin resistance and such resistance compounds the metabolic impact of diet-induced obesity. Results from multiple studies demonstrate that (1) chronically elevated central leptin decreases hypothalamic leptin receptor expression and protein levels and impairs leptin signaling; (2) leptin resistance and obesity are associated with reduced leptin receptors and diminished maximal leptin signaling capacity; and (3) leptin resistance confers increased susceptibility to diet-induced obesity. In essence, the augmented leptin accompanying obesity contributes to leptin resistance, and this leptin resistance promotes further obesity, leading to a vicious cycle of escalating metabolic devastation.
MeSH term(s)	Age Factors ; Animals ; Body Weight/physiology ; Dietary Fats/metabolism ; Energy Metabolism/physiology ; Humans ; Hypothalamus/metabolism ; Leptin/blood ; Mice ; Mice, Transgenic ; Obesity/blood ; Receptors, Cell Surface/metabolism ; Receptors, Leptin ; Signal Transduction/physiology
Chemical Substances	Dietary Fats ; LEPR protein, human ; Leptin ; Receptors, Cell Surface ; Receptors, Leptin ; leptin receptor, mouse
Language	English
Publishing date	2006-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	3907-x
ISSN	1873-507X ; 0031-9384
ISSN (online)	1873-507X
ISSN	0031-9384
DOI	10.1016/j.physbeh.2006.05.038
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Zs.A 747: Show issues

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Article ; Online: iBAT sympathetic innervation is not required for body weight loss induced by central leptin delivery.

Côté, Isabelle / Sakarya, Yasemin / Green, Sara M / Morgan, Drake / Carter, Christy S / Tümer, Nihal / Scarpace, Philip J

American journal of physiology. Endocrinology and metabolism

2017 Volume 314, Issue 3, Page(s) E224–E231

Abstract: We evaluated the contribution of brown adipose tissue (BAT) sympathetic innervation on central leptin-mediated weight loss. In a short- and long-term study, F344BN rats were submitted to either a denervation of interscapular BAT (Denervated) or a sham ... ...

Abstract	We evaluated the contribution of brown adipose tissue (BAT) sympathetic innervation on central leptin-mediated weight loss. In a short- and long-term study, F344BN rats were submitted to either a denervation of interscapular BAT (Denervated) or a sham operation (Sham). Animals from each group received the Ob (Leptin) or green fluorescent protein (GFP; Control) gene through a single injection of recombinant adeno-associated virus delivered centrally. Changes in body weight were recorded for 14 or 35 days, after which adipose tissues and skeletal muscles were weighed. In both studies, hypothalamic phosphorylated STAT3 (P-STAT3) was significantly higher in Sham-Leptin and Denervated-Leptin groups compared with their respective Control groups ( P < 0.01), indicating that leptin signaling was enhanced at the end point. We measured uncoupling protein 1 (UCP1), a marker of BAT thermogenic activity, and found a significant induction in Leptin in Sham animals ( P < 0.001) but not in Denervated animals, demonstrating that BAT UCP1 protein was only induced in Sham rats. Both Sham-Leptin and Denervated-Leptin rats lost ~15% of their initial body weight ( P < 0.001) by day 14 and reached a maximum of 18% body weight loss that stabilized over week 3 of treatment, indicating that sympathetic outflow to BAT is not required for leptin-mediated weight loss. In summary, interscapular BAT (iBAT) denervation did not prevent body weight loss following central leptin gene delivery. The present data show that sympathetic innervation of iBAT is not essential for leptin-induced body weight loss.
MeSH term(s)	Adipose Tissue, Brown/innervation ; Adipose Tissue, Brown/metabolism ; Animals ; Body Weight/genetics ; Denervation ; Dependovirus/genetics ; Gene Expression Regulation ; Gene Transfer Techniques ; Infusions, Intraventricular ; Leptin/administration & dosage ; Leptin/genetics ; Male ; Rats ; Rats, Inbred F344 ; Rats, Transgenic ; Sympathetic Nervous System/physiology ; Thermogenesis/drug effects ; Thermogenesis/genetics ; Uncoupling Protein 1/metabolism ; Weight Loss/genetics ; Weight Loss/physiology
Chemical Substances	Leptin ; Ucp1 protein, rat ; Uncoupling Protein 1
Language	English
Publishing date	2017-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00219.2017
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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