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Article ; Online: Neuroendocrine control of energy homeostasis: update on new insights.

Kalra, Satya P / Kalra, Pushpa S

2010 Volume 181, Page(s) 17–33

Abstract: Recent upsurge in research has uncovered distinct circuitries that regulate appetite, energy expenditure and fat accrual under the supervision of hormonal feedback signalling of adipocyte leptin and gastric ghrelin in the hypothalamic integration of ... ...

Abstract	Recent upsurge in research has uncovered distinct circuitries that regulate appetite, energy expenditure and fat accrual under the supervision of hormonal feedback signalling of adipocyte leptin and gastric ghrelin in the hypothalamic integration of energy homeostasis. A host of messenger molecules of diverse chemical composition and origin mediate the crosstalk between the three circuitries. Leptin is now recognized as the mandatory afferent signal in maintenance of weight homeostasis. Leptin insufficiency in the hypothalamus due to diminished transport of leptin across the blood-brain barrier (BBB) imposed by environmental causes, such as consumption of energy-enriched diets and diminished energy expenditure, orchestrates unregulated fat accrual and the attendant disease cluster of metabolic syndrome. Bioavailability of leptin selectively in the hypothalamic targets with the aid of gene therapy successfully averted the environmentally induced metabolic afflictions and normalized lifespan. Thus, sustenance of optimal sufficiency in leptin signalling solely in the hypothalamus is a novel strategy to combat the worldwide epidemic of obesity and metabolic syndrome.
MeSH term(s)	Animals ; Appetite/physiology ; Body Weight ; Energy Metabolism/physiology ; Ghrelin/metabolism ; Homeostasis/physiology ; Humans ; Hypothalamus/anatomy & histology ; Hypothalamus/metabolism ; Leptin/genetics ; Leptin/metabolism ; Metabolic Syndrome/physiopathology ; Neurosecretory Systems/physiology ; Obesity/physiopathology ; Signal Transduction/physiology
Chemical Substances	Ghrelin ; Leptin
Language	English
Publishing date	2010
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1875-7855 ; 0079-6123
ISSN (online)	1875-7855
ISSN	0079-6123
DOI	10.1016/S0079-6123(08)81002-3
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Article: To subjugate NPY is to improve the quality of life and live longer.

Kalra, Satya P / Kalra, Pushpa S

Peptides

2007 Volume 28, Issue 2, Page(s) 413–418

Abstract: The interactive network of neuropeptide Y (NPY) and cohorts is necessary for integrating the hypothalamic regulation of appetite and energy expenditure with the endocrine and neuroendocrine systems on a daily basis. Genetic and environmental factors that ...

Abstract	The interactive network of neuropeptide Y (NPY) and cohorts is necessary for integrating the hypothalamic regulation of appetite and energy expenditure with the endocrine and neuroendocrine systems on a daily basis. Genetic and environmental factors that produce an insufficiency of leptin restraint on NPY and cognate receptors deregulate the homeostasis to engender various life-threatening risk factors. Recent studies from our laboratory show that neurotherapy consisting of a single central administration of recombinant adeno-associated virus vector encoding the leptin gene can repress the hypothalamic NPY system for the lifetime of rodents. A major benefit of this stable tonic restraint is deceleration of pathophysiologic sequalae that shorten life span. These include suppression of weight gain, fat accumulation, circulating adipokines, amelioration of major symptoms of metabolic syndrome, improved reproduction and bone health. Thus, sustained repression of NPY signaling in the hypothalamus by leptin transgene expression can improve the quality of life and extend longevity.
MeSH term(s)	Appetite ; Genetic Therapy ; Humans ; Hypothalamus/physiology ; Leptin/genetics ; Neuropeptide Y/antagonists & inhibitors ; Neuropeptide Y/physiology ; Quality of Life
Chemical Substances	Leptin ; Neuropeptide Y
Language	English
Publishing date	2007-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2006.08.039
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Article: Subjugation of hypothalamic NPY and cohorts with central leptin gene therapy alleviates dyslipidemia, insulin resistance, and obesity for life-time.

Kalra, Satya P / Kalra, Pushpa S

EXS

2005 , Issue 95, Page(s) 157–169

Abstract: An interactive network comprised of neuropeptide Y (NPY) and cohorts is obligatory in the hypothalamic integration of appetite and energy expenditure on a minute-to-minute basis. High or low abundance of NPY and cognate receptors dysregulates the ... ...

Abstract	An interactive network comprised of neuropeptide Y (NPY) and cohorts is obligatory in the hypothalamic integration of appetite and energy expenditure on a minute-to-minute basis. High or low abundance of NPY and cognate receptors dysregulates the homeostatic milieu engendering hyperphagia, decreased energy expenditure, obesity and attendant metabolic syndrome cluster of dyslipidemia, glucose intolerance, insulin resistance and hyperinsulinemia, risk factors for type II diabetes and cardiovascular diseases. Increasing the supply of the endogenous repressor hormone leptin locally in the hypothalamus with the aid of leptin gene therapy, blocked age-related and dietary obesities, and the sequential development of dyslipidemia, hyperglycemia, and insulin resistance. Thus, sustained repression of NPY signaling with increased leptin selectively in the hypothalamus can avert environmental obesity and the risks of metabolic diseases.
MeSH term(s)	Animals ; Dyslipidemias/metabolism ; Dyslipidemias/therapy ; Genetic Therapy/methods ; Humans ; Hypothalamus/metabolism ; Insulin Resistance/genetics ; Insulin Resistance/physiology ; Leptin/genetics ; Leptin/metabolism ; Metabolic Syndrome/metabolism ; Metabolic Syndrome/therapy ; Neuropeptide Y/antagonists & inhibitors ; Neuropeptide Y/physiology ; Obesity/genetics ; Obesity/therapy
Chemical Substances	Leptin ; Neuropeptide Y
Language	English
Publishing date	2005-10-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1023-294X
ISSN	1023-294X
DOI	10.1007/3-7643-7417-9_12
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Article: Gene-transfer technology: a preventive neurotherapy to curb obesity, ameliorate metabolic syndrome and extend life expectancy.

Kalra, Satya P / Kalra, Pushpa S

Trends in pharmacological sciences

2005 Volume 26, Issue 10, Page(s) 488–495

Abstract: Leptin insufficiency at crucial target sites in the hypothalamic circuitries that integrate energy intake and expenditure underlies abnormal rates of fat accumulation. The payload of this "fat burden" is metabolic syndrome, a cluster of life-threatening ... ...

Abstract	Leptin insufficiency at crucial target sites in the hypothalamic circuitries that integrate energy intake and expenditure underlies abnormal rates of fat accumulation. The payload of this "fat burden" is metabolic syndrome, a cluster of life-threatening metabolic afflictions, and a shorter lifespan. Currently available therapies employed to combat obesity have disadvantages such as poor compliance for lifestyle modification or transient effectiveness and undesirable side-effects of pharmacological interventions. Recent studies suggest that neurotherapy comprising a single central administration of recombinant adeno-associated virus vector encoding the leptin gene severely depletes fat and ameliorates the major symptoms of metabolic syndrome for extended periods in rodents. These persistent benefits avert the deleterious impact of the "fat burden" and extend life expectancy. Thus, the novel approach of central gene-transfer technology has distinct advantages over current therapies and has the potential to correct or slow the progression of inherited or acquired hypothalamic diseases.
MeSH term(s)	Adenoviridae/genetics ; Animals ; Genetic Therapy/methods ; Genetic Vectors ; Humans ; Leptin/biosynthesis ; Leptin/genetics ; Life Expectancy/trends ; Metabolic Diseases/genetics ; Metabolic Diseases/metabolism ; Metabolic Diseases/therapy ; Obesity/genetics ; Obesity/metabolism ; Obesity/therapy
Chemical Substances	Leptin
Language	English
Publishing date	2005-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	282846-7
ISSN	1873-3735 ; 0165-6147
ISSN (online)	1873-3735
ISSN	0165-6147
DOI	10.1016/j.tips.2005.08.008
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Zs.A 1513: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Overlapping and interactive pathways regulating appetite and craving.

Kalra, Satya P / Kalra, Pushpa S

Journal of addictive diseases

2004 Volume 23, Issue 3, Page(s) 5–21

Abstract: Multidisciplinary research in recent years has delineated the hypothalamic hardcore wiring that encodes appetitive drive. The appetite regulating network (ARN) consisting of distinct orexigenic and anorexigenic circuitries operates in the arcuate nucleus- ...

Abstract	Multidisciplinary research in recent years has delineated the hypothalamic hardcore wiring that encodes appetitive drive. The appetite regulating network (ARN) consisting of distinct orexigenic and anorexigenic circuitries operates in the arcuate nucleus-paraventricular nucleus axis of the hypothalamus to propagate and relay the appetitive drive, and is subject to modulation by excitatory and inhibitory messages from the lateral hypothalamus and ventromedial nucleus, respectively. Reciprocal afferent humoral signals, comprised of anorexigenic leptin from white adipose tissue and orexigenic ghrelin from stomach, to the ARN integrate the moment-to-moment regulation of energy homeostasis. Various loci in the ARN and afferent hormonal feedback circuitry in the rodent brain are important for food craving elicited by drugs of abuse. This convergence of neurochemical and hormonal signaling has now paved the way to address the fundamental question of whether cellular and molecular events that underlie the appetitive drive in response to diminished energy stores in the body are akin to drug craving during withdrawal in humans.
MeSH term(s)	Adipose Tissue/physiology ; Appetite Regulation/drug effects ; Appetite Regulation/physiology ; Body Weight/drug effects ; Cannabinoid Receptor Modulators/physiology ; Energy Intake/physiology ; Ghrelin ; Humans ; Hypothalamus/physiology ; Intracellular Signaling Peptides and Proteins/physiology ; Leptin/physiology ; Narcotics/pharmacology ; Neuropeptides/physiology ; Nicotine/pharmacology ; Orexins ; Peptide Hormones/physiology ; Signal Transduction/physiology ; Stomach/physiology ; Ventromedial Hypothalamic Nucleus/physiology ; gamma-Aminobutyric Acid/physiology
Chemical Substances	Cannabinoid Receptor Modulators ; Ghrelin ; Intracellular Signaling Peptides and Proteins ; Leptin ; Narcotics ; Neuropeptides ; Orexins ; Peptide Hormones ; gamma-Aminobutyric Acid (56-12-2) ; Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2004
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1077616-3
ISSN	1055-0887
ISSN	1055-0887
DOI	10.1300/J069v23n03_02
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Zs.A 1696: Show issues

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Article: NPY--an endearing journey in search of a neurochemical on/off switch for appetite, sex and reproduction.

Kalra, Satya P / Kalra, Pushpa S

Peptides

2004 Volume 25, Issue 3, Page(s) 465–471

Abstract: Although a dynamic link between the two innate drives, appetite for food and the urge to reproduce, in vertebrate evolution has been known for a long time, a distinct neurochemical pathway mediating this integration has only recently been appreciated. ... ...

Abstract	Although a dynamic link between the two innate drives, appetite for food and the urge to reproduce, in vertebrate evolution has been known for a long time, a distinct neurochemical pathway mediating this integration has only recently been appreciated. Study of the precise anatomy of the neural track began in the early to mid 20th century after the sites of genesis of the two instincts were localized to the hypothalamus. This report narrates the birth and fruition to maturity of insights into the commonality of hypothalamic neuropeptide Y (NPY) signaling for the two instinctual drives along two distinct pathways.
MeSH term(s)	Animals ; Appetite/physiology ; Humans ; Hypothalamus/physiology ; Neuropeptide Y/physiology ; Sexual Behavior/physiology ; Sexual Behavior, Animal/physiology
Chemical Substances	Neuropeptide Y
Language	English
Publishing date	2004-03
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2004.03.001
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Article: Obesity and metabolic syndrome: long-term benefits of central leptin gene therapy.

Kalra, Pushpa S / Kalra, Satya P

Drugs of today (Barcelona, Spain : 1998)

2003 Volume 38, Issue 11, Page(s) 745–757

Abstract: The recent rapid rise in the incidence of obesity has prompted investigations into understanding the hormonal and neuronal pathways involved in body weight homeostasis in order to devise novel therapeutic strategies. The early enthusiasm for the ... ...

Abstract	The recent rapid rise in the incidence of obesity has prompted investigations into understanding the hormonal and neuronal pathways involved in body weight homeostasis in order to devise novel therapeutic strategies. The early enthusiasm for the adipocyte hormone leptin as a regulator of fat mass was largely discarded because of the apparent development of leptin resistance, as seen in obese subjects with elevated blood leptin levels. We postulated that this leptin ineffectiveness may be caused by a lack of leptin availability at target sites in the hypothalamus. To test this hypothesis, we used viral vectors to introduce the leptin gene into the brain for a sustained supply of leptin in the hypothalamus. A single injection of recombinant adeno-associated virus encoding the leptin gene (rAAV-lep) into the third cerebroventricle prevented the aging-associated gradual increase in body weight and adiposity in adult rats for 6 months of the experiment. When administered to prepubertal rats, significantly lower body weight gain and adiposity were maintained for up to 10 months of the experiment. In addition, obesity was prevented in rats introduced to a high-fat diet and also reversed in obese-prone rats maintained on a high-fat diet. Body weight homeostasis and loss of adiposity by leptin gene therapy was achieved by an increase in energy expenditure, and when the rAAV-lep titer was increased, there was also a voluntary reduction in food intake. Importantly, this therapy reduced blood levels of insulin, triglycerides and free fatty acids, the pathophysiologic correlates of the metabolic syndrome. Thus, the long-term beneficial effects of central leptin gene therapy may herald the development of newer therapeutic strategies to control the epidemic of obesity and related metabolic disorders.
MeSH term(s)	Adenoviridae/genetics ; Age Factors ; Animals ; Dependovirus/genetics ; Dietary Fats/adverse effects ; Energy Metabolism ; Genetic Therapy/methods ; Genetic Vectors ; Ghrelin ; Humans ; Leptin/deficiency ; Leptin/genetics ; Leptin/metabolism ; Metabolic Diseases/etiology ; Metabolic Diseases/metabolism ; Metabolic Diseases/therapy ; Obesity/etiology ; Obesity/metabolism ; Obesity/therapy ; Peptide Hormones/metabolism ; Syndrome
Chemical Substances	Dietary Fats ; Ghrelin ; Leptin ; Peptide Hormones
Language	English
Publishing date	2003-02-11
Publishing country	Spain
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ISSN	1699-3993
ISSN	1699-3993
DOI	10.1358/dot.2002.38.11.740201
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Article: Neuropeptide Y: a physiological orexigen modulated by the feedback action of ghrelin and leptin.

Kalra, Satya P / Kalra, Pushpa S

Endocrine

2003 Volume 22, Issue 1, Page(s) 49–56

Abstract: Neuropeptide Y (NPY), a 36-amino-acid neuropeptide is the most potent physiological appetite transducer known. Episodic NPY neurosecretion in hypothalamic target sites is temporally linked with onset of the daily feeding pattern. Upregulation of NPY ... ...

Abstract	Neuropeptide Y (NPY), a 36-amino-acid neuropeptide is the most potent physiological appetite transducer known. Episodic NPY neurosecretion in hypothalamic target sites is temporally linked with onset of the daily feeding pattern. Upregulation of NPY signaling in the arcuate nucleus-paraventricular nucleus (ARC-PVN) neural axis is responsible for the hyperphagia evoked by dieting, fasting, hormonal and genetic factors, and disruption in intrahypothalamic signaling. Clusters of NPY-producing neurons in the ARC that coexpress gamma- amino butyric acid and agouti-related peptide, and those in the brain stem (BS) that coexpress catecholamines and galanin, participate in disparate manners to regulate appetitive behavior. NPY receptors, Y1, Y2, and Y5, expressed by various components of the NPY network, mediate NPY-induced feeding. Imbalance in NPY signaling due either to high or low abundance of NPY at target sites elicits hyperphagia leading to increased fat accretion and obesity. Recent studies show that intermittent, feedback action of opposing afferent hormonal signals-leptin from adipose tissue and ghrelin from stomach-regulate the episodic secretion of orexigenic NPY in the PVN-ARC. Apparently, the hypothalamic NPY network is the primary common pathway intimately involved in genesis of appetite- stimulating impulses.
MeSH term(s)	Animals ; Appetite/drug effects ; Appetite/physiology ; Appetite Stimulants/pharmacology ; Feeding and Eating Disorders/physiopathology ; Humans ; Neuropeptide Y/pharmacology ; Neuropeptide Y/physiology ; Neuropeptide Y/secretion ; Obesity/physiopathology
Chemical Substances	Appetite Stimulants ; Neuropeptide Y
Language	English
Publishing date	2003-10
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1194484-5
ISSN	1355-008X ; 0969-711X
ISSN	1355-008X ; 0969-711X
DOI	10.1385/ENDO:22:1:49
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Article: Low abundance of NPY in the hypothalamus can produce hyperphagia and obesity.

Dube, Michael G / Kalra, Satya P / Kalra, Pushpa S

Peptides

2007 Volume 28, Issue 2, Page(s) 475–479

Abstract: States of increased metabolic demand are associated with up-regulation of NPY and hyperphagia. However, we present some instances of hyperphagia in which NPY is not up-regulated. Ablation or functional disruption of specific sites in the hypothalamus, ... ...

Abstract	States of increased metabolic demand are associated with up-regulation of NPY and hyperphagia. However, we present some instances of hyperphagia in which NPY is not up-regulated. Ablation or functional disruption of specific sites in the hypothalamus, such as the ventromedial or paraventricular nuclei, or transection of inputs to the hypothalamus from the hindbrain results in hyperphagia and excess body weight gain. However, NPY expression and concentration in these experimental models is either decreased or unchanged. While there is no up-regulation of NPY in these models, there is increased sensitivity to the orexigenic effects of NPY. This enhanced responsiveness to NPY may more than compensate for the reduced levels of NPY and result in hyperphagia and excess body weight gain. The hyper-responsiveness may be due either to an increase in NPY receptors or to other changes in target cells and response pathways that may result from the treatments used in these models.
MeSH term(s)	Humans ; Hyperphagia/metabolism ; Hypothalamus/metabolism ; Neuropeptide Y/metabolism ; Obesity/metabolism
Chemical Substances	Neuropeptide Y
Language	English
Publishing date	2007-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2006.10.017
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Zs.A 1649: Show issues

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Article: The hypothalamic paraventricular nucleus is not essential for orexigenic NPY or anorexigenic melanocortin action.

Dube, Michael G / Kalra, Satya P / Kalra, Pushpa S

Peptides

2006 Volume 27, Issue 9, Page(s) 2239–2248

Abstract: Bilateral electrolytic lesions of the paraventricular nucleus of the hypothalamus (PVN) produce hyperphagia with excess weight gain. The orexigenic neuropeptide Y (NPY) system and the anorexigenic melanocortin system act in the PVN to regulate food ... ...

Abstract	Bilateral electrolytic lesions of the paraventricular nucleus of the hypothalamus (PVN) produce hyperphagia with excess weight gain. The orexigenic neuropeptide Y (NPY) system and the anorexigenic melanocortin system act in the PVN to regulate food intake, and participate in mediating the anorexic effects of leptin. We hypothesized that changes in the responsiveness of these systems may contribute to the hyperphagia observed in PVN-lesioned rats. Adult female Sprague-Dawley rats received either sham or electrolytic lesions in the PVN immediately followed by implantation of a guide cannula into the third cerebroventricle. Twenty-five days following surgery groups of sham and hyperphagic PVN-lesioned rats were injected intracerebroventricularly (i.c.v.) with either 118 pmole or 470 pmole of NPY and food intake was measured for 3 h. Food intake in response to NPY was nearly three-fold higher in PVN-lesioned rats as compared to sham rats. However, the response to 5 microg leptin i.c.v. was not different in lesioned versus sham rats. The effect of the melanocortin agonist MTII on food intake was tested in additional rats beginning either 7-14 days or 30-40 days following surgery. Doses of 0.1 nmole or 1.0 nmole of MTII were injected immediately before lights-off and food intake was measured at 2 h, 24 h and 48 h post-injection. Suppression of food intake in PVN-lesioned rats was not different from that in sham-lesioned rats. These data suggest that hyper-responsiveness to NPY may account in part for the hyperphagia observed in PVN-lesioned rats. Furthermore, based on the similarities of responses of PVN-lesioned and sham control rats to the anorexigenic agents MTII and leptin and the hypersensitivity of lesioned rats to NPY, we conclude that the PVN is not essential for NPY stimulation of food intake or for melanocortin suppression of food intake and that NPY and melanocortin receptors outside of the PVN are sufficient to produce these effects.
MeSH term(s)	Animals ; Body Weight/drug effects ; Eating/drug effects ; Female ; Leptin/administration & dosage ; Leptin/pharmacology ; Neuropeptide Y/pharmacology ; Paraventricular Hypothalamic Nucleus/cytology ; Paraventricular Hypothalamic Nucleus/drug effects ; Paraventricular Hypothalamic Nucleus/physiology ; Rats ; Rats, Sprague-Dawley ; Receptor, Melanocortin, Type 3/agonists ; Receptor, Melanocortin, Type 3/metabolism ; Time Factors ; alpha-MSH/analogs & derivatives ; alpha-MSH/pharmacology
Chemical Substances	Leptin ; Neuropeptide Y ; Receptor, Melanocortin, Type 3 ; acetyl-norleucyl(4)-(aspartyl(5)-histidyl(6)-phenylalanyl(7)-arginyl(8)-tryptophyl(9)-lysyl(10))cyclo-alpha-MSH(4-10)amide ; alpha-MSH (581-05-5)
Language	English
Publishing date	2006-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2006.04.005
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