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Ability of insulin to modulate hepatic glucose production in aging rats is impaired by fat accumulation.

https://arctichealth.org/en/permalink/ahliterature61796
Source
Am J Physiol Endocrinol Metab. 2000 Jun;278(6):E985-91
Publication Type
Article
Date
Jun-2000
Author
G. Gupta
J A Cases
L. She
X H Ma
X M Yang
M. Hu
J. Wu
L. Rossetti
N. Barzilai
Author Affiliation
Department of Medicine, and the Diabetes Research and Training Center, Albert Einstein College of Medicine, New York, New York 10461, USA.
Source
Am J Physiol Endocrinol Metab. 2000 Jun;278(6):E985-91
Date
Jun-2000
Language
English
Publication Type
Article
Keywords
Adipose Tissue
Aging
Animals
Body Composition
Energy intake
Gluconeogenesis
Glucose - biosynthesis
Glycogen - metabolism
Insulin - pharmacology
Leptin - metabolism
Liver - drug effects - metabolism
Male
Rats
Rats, Inbred BN
Rats, Inbred F344
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Abstract
Increased total fat mass (FM) and visceral fat (VF) may account in part for age-associated decrease in hepatic insulin action. This study determined whether preventing the changes in body fat distribution abolished this defect throughout aging. We studied the F(1) hybrid of Brown Norway-Fischer 344 rats (n = 29), which we assigned to caloric restriction (CR) or fed ad libitum (AL). CR (55% of the calories consumed by AL) was initiated and used at 2 mo to prevent age-dependent increases in FM and VF. AL rats were studied at 2, 8, and 20 mo; CR rats were studied at 8 and 20 mo. VF and FM remained unchanged throughout aging in CR rats. AL-fed rats at 8 and 20 mo had over fourfold higher FM and VF compared with both CR groups. Insulin clamp studies (3 mU. kg(-1). min(-1) with somatostatin) were performed to assess hepatic insulin sensitivity. Prevention of fat accretion resulted in a marked improvement in insulin action in the suppression of hepatic glucose production (HGP) (6.3 +/- 0.3 and 7.2 +/- 1.2 mg. kg(-1). min(-1) in 8- and 20-mo CR rats vs. 8.3 +/- 0.5 and 10.8 +/- 0.9 mg. kg(-1). min(-1) in 8- and 20-mo AL rats, respectively). The rate of gluconeogenesis (by enrichment of hepatic uridine diphosphate glucose and phosphoenolpyruvate pools by [(14)C]lactate) was unchanged in all groups. The improvement in hepatic insulin action in the CR group was mostly due to effective suppression of glycogenolysis (4.4 +/- 0.3 and 4.9 +/- 0.3 mg. kg(-1). min(-1) in 8- and 20-mo CR rats vs. 5.8 +/- 0.6 and 8.2 +/- 1.0 mg. kg(-1). min(-1) in 8- and 20-mo AL rats, respectively). The results demonstrated the preservation of hepatic insulin action in aging CR rats. Therefore, body fat and its distribution are major determinants of age-associated hepatic insulin resistance.
PubMed ID
10826999 View in PubMed
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Adipocytokines, C-reactive protein, and cardiovascular disease: a population-based prospective study.

https://arctichealth.org/en/permalink/ahliterature272267
Source
PLoS One. 2015;10(6):e0128987
Publication Type
Article
Date
2015
Author
Ekim Seven
Lise L N Husemoen
Thomas S G Sehested
Hans Ibsen
Kristian Wachtell
Allan Linneberg
Jørgen L Jeppesen
Source
PLoS One. 2015;10(6):e0128987
Date
2015
Language
English
Publication Type
Article
Keywords
Adipokines - metabolism
Adult
Aged
Blood pressure
C-Reactive Protein - metabolism
Cardiovascular Diseases - epidemiology - etiology - metabolism
Denmark - epidemiology
Early Medical Intervention
Female
Humans
Incidence
Insulin Resistance
Leptin - metabolism
Longitudinal Studies
Male
Middle Aged
Obesity - complications
Prognosis
Prospective Studies
Risk factors
Abstract
Being overweight or obese is associated with a greater risk of coronary heart disease and stroke compared with normal weight. The role of the specific adipose tissue-derived substances, called adipocytokines, in overweight- and obesity-related cardiovascular disease (CVD) is still unclear.
To investigate the associations of three adipose tissue-derived substances: adiponectin, leptin, and interleukin-6 with incident CVD in a longitudinal population-based study, including extensive adjustments for traditional and metabolic risk factors closely associated with overweight and obesity. C-reactive protein (CRP) was used as a proxy for interleukin-6.
Prospective population-based study of 6.502 participants, 51.9% women, aged 30-60 years, free of CVD at baseline, with a mean follow-up time of 11.4 years, equivalent to 74,123 person-years of follow-up. As outcome, we defined a composite outcome comprising of the first event of fatal and nonfatal coronary heart disease and fatal and nonfatal stroke.
During the follow-up period, 453 composite CV outcomes occurred among participants with complete datasets. In models, including gender, age, smoking status, systolic blood pressure, treatment for hypertension, diabetes, body mass index (BMI), total cholesterol, high-density-lipoprotein cholesterol, homeostasis model assessment of insulin resistance, estimated glomerular filtration rate, adiponectin, leptin, and CRP, neither adiponectin (hazard ratio [HR] with 95% confidence interval [CI]: 0.97 [0.87-1.08] per SD increase, P = 0.60) nor leptin (0.97 [0.85-1.12] per SD increase, P = 0.70) predicted the composite outcome, whereas CRP was significantly associated with the composite outcome (1.19 [1.07-1.35] per SD increase, P = 0.002). Furthermore, in mediation analysis, adjusted for age and sex, CRP decreased the BMI-associated CV risk by 43% (95%CI 29-72).
In this study, neither adiponectin nor leptin were independently associated with CVD, raising questions over their role in CVD. The finding that CRP was significantly associated with an increased risk of CVD and decreased the BMI-associated CVD risk substantially, could imply that interleukin-6-related pathways may play a role in mediating overweight- and obesity-related CVD.
Notes
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PubMed ID
26035431 View in PubMed
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Adipokine genes and prostate cancer risk.

https://arctichealth.org/en/permalink/ahliterature154045
Source
Int J Cancer. 2009 Feb 15;124(4):869-76
Publication Type
Article
Date
Feb-15-2009
Author
Moore SC
Leitzmann MF
Albanes D
Weinstein SJ
Snyder K
Virtamo J
Ahn J
Mayne ST
Yu H
Peters U
Gunter MJ
Author Affiliation
Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA. moorest@mail.nih.gov
Source
Int J Cancer. 2009 Feb 15;124(4):869-76
Date
Feb-15-2009
Language
English
Publication Type
Article
Keywords
Adipokines - metabolism
Adiponectin - metabolism
Aged
Case-Control Studies
Cohort Studies
Cytokines - metabolism
Finland
Humans
Insulin - metabolism
Insulin-Like Growth Factor I - metabolism
Interleukin-6 - metabolism
Leptin - metabolism
Linkage Disequilibrium
Male
Middle Aged
Prostatic Neoplasms - epidemiology - metabolism - pathology
Receptors, Leptin - metabolism
Risk
Tumor Necrosis Factor-alpha - metabolism
Abstract
Adiposity and adipocyte-derived cytokines have been implicated in prostate carcinogenesis. However, the relationship of adipokine gene variants with prostate cancer risk has not been thoroughly investigated. We therefore examined common variants of the IL6, LEP, LEPR, TNF and ADIPOQ genes in relation to prostate cancer in a case-control study nested within a large cohort of Finnish men. The study sample consisted of 1,053 cases of prostate cancer, diagnosed over an average 11 years of follow up, and 1,053 controls matched to the cases on age, intervention group and date of baseline blood draw. Logistic regression was used to model the relative odds of prostate cancer. We also examined genotypes in relation to serum insulin, IGF-1 and IGF-1:IGFBP-3 among 196 controls. Variant alleles at three loci (-14858A>G, -13973A>C, -13736C>A) in a potential regulatory region of the LEP gene conferred a statistically significant 20% reduced risk of prostate cancer. For example, at the -14858A>G locus, heterozygotes and homozygotes for the A allele had an odds ratio (OR) of prostate cancer of 0.76 [95% confidence interval (CI) 0.62, 0.93] and 0.79 (95% CI 0.60, 1.04), respectively. At 13288G>A, relative to the GG genotype, the AA genotype was associated with a suggestive increased risk of prostate cancer (OR = 1.29; 95% CI 0.99,1.67; p(trend) = 0.05). Polymorphisms in the IL6, LEPR, TNF and ADIPOQ genes were not associated with prostate cancer. Allelic variants in the LEP gene are related to prostate cancer risk, supporting a role for leptin in prostate carcinogenesis.
Notes
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PubMed ID
19035456 View in PubMed
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Adipose tissue density, a novel biomarker predicting mortality risk in older adults.

https://arctichealth.org/en/permalink/ahliterature113601
Source
J Gerontol A Biol Sci Med Sci. 2014 Jan;69(1):109-17
Publication Type
Article
Date
Jan-2014
Author
Rachel A Murphy
Thomas C Register
Carol A Shively
J Jeffrey Carr
Yaorong Ge
Marta E Heilbrun
Steven R Cummings
Annemarie Koster
Michael C Nevitt
Suzanne Satterfield
Frances A Tylvasky
Elsa S Strotmeyer
Anne B Newman
Eleanor M Simonsick
Ann Scherzinger
Bret H Goodpaster
Lenore J Launer
Gudny Eiriksdottir
Sigurdur Sigurdsson
Gunnar Sigurdsson
Vilmundur Gudnason
Thomas F Lang
Stephen B Kritchevsky
Tamara B Harris
Author Affiliation
Laboratory of Population Science, National Institute on Aging, 7201 Wisconsin Ave, 3C-309 Bethesda, MD 20814. rachel.murphy@nih.gov.
Source
J Gerontol A Biol Sci Med Sci. 2014 Jan;69(1):109-17
Date
Jan-2014
Language
English
Publication Type
Article
Keywords
Absorptiometry, Photon
Adiponectin - metabolism
Adipose Tissue - metabolism - radiography
Aged
Aged, 80 and over
Aging - physiology
Animals
Biological Markers - metabolism
Body mass index
Female
Follow-Up Studies
Humans
Leptin - metabolism
Macaca fascicularis
Male
Obesity - metabolism - mortality - radiography
Prognosis
Prospective Studies
Risk factors
Survival Rate - trends
Abstract
Knowledge of adipose composition in relation to mortality may help delineate inconsistent relationships between obesity and mortality in old age. We evaluated relationships between abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) density, mortality, biomarkers, and characteristics.
VAT and SAT density were determined from computed tomography scans in persons aged 65 and older, Health ABC (n = 2,735) and AGES-Reykjavik (n = 5,131), and 24 nonhuman primates (NHPs). Associations between adipose density and mortality (4-13 years follow-up) were assessed with Cox proportional hazards models. In NHPs, adipose density was related to serum markers and tissue characteristics.
Higher density adipose tissue was associated with mortality in both studies with adjustment for risk factors including adipose area, total fat, and body mass index. In women, hazard ratio and 95% CI for the densest quintile (Q5) versus least dense (Q1) for VAT density were 1.95 (1.36-2.80; Health ABC) and 1.88 (1.31-2.69; AGES-Reykjavik) and for SAT density, 1.76 (1.35-2.28; Health ABC) and 1.56 (1.15-2.11; AGES-Reykjavik). In men, VAT density was associated with mortality in Health ABC, 1.52 (1.12-2.08), whereas SAT density was associated with mortality in both Health ABC, 1.58 (1.21-2.07), and AGES-Reykjavik, 1.43 (1.07-1.91). Higher density adipose tissue was associated with smaller adipocytes in NHPs. There were no consistent associations with inflammation in any group. Higher density adipose tissue was associated with lower serum leptin in Health ABC and NHPs, lower leptin mRNA expression in NHPs, and higher serum adiponectin in Health ABC and NHPs.
VAT and SAT density provide a unique marker of mortality risk that does not appear to be inflammation related.
PubMed ID
23707956 View in PubMed
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Helicobacter pylori persistence: biology and disease.

https://arctichealth.org/en/permalink/ahliterature181728
Source
J Clin Invest. 2004 Feb;113(3):321-33
Publication Type
Article
Date
Feb-2004
Author
Martin J Blaser
John C Atherton
Author Affiliation
Department of Medicine, New York University School of Medicine, and New York Harbor Veterans Affairs Medical Center, New York 10016, USA. martin.blaser@med.nyu.edu
Source
J Clin Invest. 2004 Feb;113(3):321-33
Date
Feb-2004
Language
English
Publication Type
Article
Keywords
Ghrelin
Helicobacter Infections - immunology - metabolism - physiopathology
Helicobacter pylori - immunology - metabolism - pathogenicity
Humans
Inflammation - immunology - metabolism - microbiology
Leptin - metabolism
Peptide Hormones - metabolism
Stomach - microbiology
Stomach Diseases - microbiology - physiopathology
Virulence
Abstract
Helicobacter pylori are bacteria that have coevolved with humans to be transmitted from person to person and to persistently colonize the stomach. Their population structure is a model for the ecology of the indigenous microbiota. A well-choreographed equilibrium between bacterial effectors and host responses permits microbial persistence and health of the host but confers risk of serious diseases, including peptic ulceration and gastric neoplasia.
Notes
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PubMed ID
14755326 View in PubMed
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High leptin levels are associated with stroke.

https://arctichealth.org/en/permalink/ahliterature47448
Source
Cerebrovasc Dis. 2003;15(1-2):63-9
Publication Type
Article
Date
2003
Author
Stefan Söderberg
Birgitta Stegmayr
Christine Ahlbeck-Glader
Lisbeth Slunga-Birgander
Bo Ahrén
Tommy Olsson
Author Affiliation
Department of Medicine, Clinical Chemistry of Umeå University, Umeå, Sweden. stefan.soderberg@medicin.umu.se
Source
Cerebrovasc Dis. 2003;15(1-2):63-9
Date
2003
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Biological Markers - blood
Blood Pressure - physiology
Brain Ischemia - epidemiology - metabolism - physiopathology
Case-Control Studies
Cerebral Hemorrhage - epidemiology - metabolism - physiopathology
Cerebrovascular Accident - epidemiology - metabolism - physiopathology
Comparative Study
Diabetes Mellitus - epidemiology - metabolism - physiopathology
Diastole - physiology
Female
Humans
Hypertension - epidemiology - metabolism - physiopathology
Length of Stay
Leptin - metabolism
Male
Middle Aged
Multivariate Analysis
Obesity - epidemiology - metabolism - physiopathology
Research Support, Non-U.S. Gov't
Risk factors
Statistics
Sweden
Systole - physiology
Abstract
BACKGROUND AND PURPOSE: Leptin, an important hormone for body weight regulation, may be involved in the pathogenesis of cardiovascular manifestations of obesity. We tested whether leptin may be an independent risk marker for stroke in a case-referent study. METHODS: Definitive acute stroke events, defined by MONICA criteria, were identified from October 1, 1995 to April 30, 1999. Referents without known cardiovascular disease were randomly selected from a population census. Patient characteristics were taken from hospital files and leptin was analyzed in stored samples. Logistic regression analysis was used to determine possible differences in leptin levels between groups. RESULTS: One hundred and thirty-seven cases with ischemic stroke and 69 cases with hemorrhagic stroke were identified. In comparison with referents, male patients with stroke had significantly higher leptin levels. Both male and female stroke patients had increased blood pressure compared with the referents. In multivariate analyses, high leptin levels were associated with both ischemic (OR = 4.89; 95% CI: 1.89-12.62) and hemorrhagic (OR = 3.86; 95% CI: 1.13-13.16) stroke in men, and with ischemic stroke in women (OR = 4.10; 95% CI: 1.45-11.62). The combination of high leptin levels and increased blood pressure (systolic or diastolic) was associated with a strong positive interaction in males with hemorrhagic stroke. CONCLUSION: Leptin may be an important link for the development of cerebrovascular disease in the insulin resistance syndrome in men.
PubMed ID
12499713 View in PubMed
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Influence of obesity on the prevalence and clinical features of asthma.

https://arctichealth.org/en/permalink/ahliterature154059
Source
Clin Invest Med. 2008;31(6):E386-90
Publication Type
Conference/Meeting Material
Date
2008
Author
Louis-Philippe Boulet
Author Affiliation
Centre de Pneumologie, Hôpital Laval,Institut Universitaire de Cardiologie et dePneumologie de l'Université Laval. lpboulet@med.ulaval.ca
Source
Clin Invest Med. 2008;31(6):E386-90
Date
2008
Language
English
Publication Type
Conference/Meeting Material
Keywords
Asthma - epidemiology - metabolism - physiopathology
Body mass index
Canada - epidemiology
Cytokines - metabolism
Humans
Leptin - metabolism
Obesity - physiopathology
Prevalence
Risk factors
Treatment Outcome
Weight Loss - physiology
Abstract
Obesity has been associated with an increased prevalence of asthma and poorer control of this disease. However, the mechanisms by which obesity can influence airway function and make asthma more difficult to control remain uncertain. The physiological changes associated with obesity can contribute to respiratory symptoms and these should be differentiated from those caused by asthma. Obesity can possibly influence the development of asthma through genetic, developmental, hormonal, neurogenic or mechanical influences. Breathing at low lung volumes and changes in the pattern of breathing in obese subjects may alter airway smooth muscle plasticity and airway function. The release by adipocytes of various cytokines and mediators such as Interleukin-6, TNF-alpha, eotaxin, and leptin, and the reduction of anti-inflammatory adipokines in obese subjects may possibly contribute to the development or increased clinical expression of asthma in promoting airway inflammation. Reduced asthma control and impaired response to asthma therapy have been reported in obese patients. Obesity-related co-morbidities such as Sleep Apnea and Gastro-esophageal reflux may also contribute to this poor control. Weight loss improves asthma control and reduces medication needs. Research is needed to better define the optimal management of obese asthmatic patients.
PubMed ID
19032910 View in PubMed
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Obesity and colon cancer: does leptin provide a link?

https://arctichealth.org/en/permalink/ahliterature17969
Source
Int J Cancer. 2004 Mar;109(1):149-52
Publication Type
Article
Date
Mar-2004
Author
Pär Stattin
Annekatrin Lukanova
Carine Biessy
Stefan Söderberg
Richard Palmqvist
Rudolf Kaaks
Tommy Olsson
Egil Jellum
Author Affiliation
Department of Urology and Andrology, Umeå University Hospital, Umeå, Sweden. par.stattin@urologi.umu.se
Source
Int J Cancer. 2004 Mar;109(1):149-52
Date
Mar-2004
Language
English
Publication Type
Article
Keywords
Adult
C-Peptide - chemistry
Case-Control Studies
Colonic Neoplasms - etiology
Colorectal Neoplasms - blood
Cryopreservation
Humans
Insulin - metabolism
Leptin - metabolism - physiology
Logistic Models
Male
Middle Aged
Obesity - etiology
Odds Ratio
Registries
Research Support, Non-U.S. Gov't
Time Factors
Abstract
Obesity, a risk factor for colorectal cancer, is associated with elevated serum levels of leptin, the adipocyte-derived hormone, and insulin. Experimental and epidemiologic studies have indicated a role for insulin in the pathogenesis of colon cancer, and recent experimental studies have suggested a similar role for leptin. In a case-control study nested in the Janus Biobank, Norway, we measured serum levels of leptin and C-peptide (a marker of pancreatic insulin secretion) in cryopreserved prediagnostic sera from men (median age, 45 years) who were diagnosed with cancer of the colon (n = 235) or rectum (n = 143) after blood collection (median time, 17 years), and among 378 controls matched for age and date of blood collection. Conditional logistic regression analyses showed an approximately 3-fold increase in colon cancer risk with increasing concentrations of leptin up to an odds ratio (OR) of 2.72 (95% CI = 1.44-5.12) for top vs. bottom quartile (p(trend) = 0.008). The corresponding OR for C-peptide was 1.81 (95% CI = 0.67-4.86; p(trend) = 0.19). The risk estimates remained unchanged after mutual adjustment. No association of hormone levels with rectal cancer risk was found. Reproducibility of hormone measurements assessed by intraclass coefficients (ICCs) for paired samples taken 1 year apart was high for leptin (ICC = 0.82) but lower for C-peptide (ICC = 0.30). Our results suggest that leptin is a risk factor for colon cancer, and that leptin may provide a link between obesity and colon cancer. Leptin may be directly involved in colon tumorigenesis or it may serve as a sensitive and robust marker of an obesity-induced adverse endocrine environment. Only weak support for an association of insulin with colon cancer was found.
PubMed ID
14735482 View in PubMed
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Reduced leptin concentrations are permissive for display of torpor in Siberian hamsters.

https://arctichealth.org/en/permalink/ahliterature57238
Source
Am J Physiol Regul Integr Comp Physiol. 2004 Jul;287(1):R97-R103
Publication Type
Article
Date
Jul-2004
Author
David A Freeman
Daniel A Lewis
Alexander S Kauffman
Robert M Blum
John Dark
Author Affiliation
Dept. of Psychology, Box 1650, Univ. of California, Berkeley, CA 94720-1650, USA.
Source
Am J Physiol Regul Integr Comp Physiol. 2004 Jul;287(1):R97-R103
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Animals
Behavior, Animal - physiology
Body Temperature - physiology
Body Weight - physiology
Cold
Cricetinae
Female
Food Deprivation - physiology
Hibernation - physiology
Leptin - metabolism - physiology
Male
Motor Activity
Phodopus
Photoperiod
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Telemetry
Abstract
A photoperiod with a short photophase induces a winterlike phenotype in Siberian hamsters that includes a progressive decrease in food intake and body mass and reproductive organ regression, as well as reversible hypothermia in the form of short-duration torpor. Torpor substantially reduces energy utilization and is not initiated until body mass, fat stores, and serum leptin concentrations are at their nadir. Because photoperiod-dependent torpor is delayed until fat reserves are lowest, leptin concentrations may be a permissive factor for torpor onset. This conjecture was tested by implanting osmotic minipumps into Siberian hamsters manifesting spontaneous torpor; the animals received a constant release of leptin or vehicle for 14 days. Exogenous leptin treatment eliminated torpor in a significant proportion of treated hamsters, whereas treatment with the vehicle did not. Similarly, endogenous serum leptin concentrations were markedly reduced in all animals undergoing daily torpor. Although simply reducing leptin concentrations below a threshold value is not sufficient for torpor initiation, reduced leptin concentrations nevertheless appear necessary for its occurrence. It is proposed that drastically reduced leptin concentrations provide a "starvation signal" to an as yet unidentified central mechanism mediating torpor initiation.
Notes
Comment In: Am J Physiol Regul Integr Comp Physiol. 2004 Jul;287(1):R6-715191922
PubMed ID
15191926 View in PubMed
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Skeletal bone morphology is resistant to the high amplitude seasonal leptin cycle in the Siberian hamster.

https://arctichealth.org/en/permalink/ahliterature83300
Source
J Endocrinol. 2005 Sep;186(3):475-9
Publication Type
Article
Date
Sep-2005
Author
Rousseau K.
Atcha Z.
Denton J.
Cagampang F R A
Ennos A R
Freemont A J
Loudon A S I
Author Affiliation
Faculties of Life Sciences, University of Manchester, UK.
Source
J Endocrinol. 2005 Sep;186(3):475-9
Date
Sep-2005
Language
English
Publication Type
Article
Keywords
Animals
Biomechanics
Body Weight - drug effects
Bone and Bones - anatomy & histology - drug effects
Cricetinae
Female
Infusions, Intravenous
Leptin - metabolism
Male
Phodopus - anatomy & histology - metabolism
Photoperiod
Reproduction - physiology
Seasons
Abstract
Recent studies have suggested that the adipocyte-derived hormone, leptin, plays a role in the regulation of metabolism. Here, we tested this hypothesis in the seasonally breeding Siberian hamster, as this species exhibits profound seasonal changes in adiposity and circulating leptin concentrations driven by the annual photoperiodic cycle. Male hamsters were kept in either long (LD) or short (SD) photoperiods. Following exposure to short photoperiods for 8 weeks animals exhibited a significant weight-loss and a 16-fold reduction of serum leptin concentrations. At Week 9, animals in both photoperiods were infused with leptin or PBS via osmotic mini-pump for 14 days. Chronic leptin infusion mimicked LD-like concentrations in SD-housed animals and caused a further decline in body weight and adipose tissue. In LD-housed animals, leptin infusion resulted in a significant elevation of serum concentrations above natural LD-like levels, but had no discernable effect on body weight or overall adiposity. Both bending and compression characteristics and histomorphometric measurements of trabecular bone mass were unaltered by leptin treatment or photoperiod. Our data therefore show that despite a high natural amplitude cycle of leptin, this hormone has no apparent role in the regulation of bone metabolism, and therefore do not support recent propositions that this hormone is an important component in the metabolism of bone tissue.
PubMed ID
16135667 View in PubMed
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