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  1. Article: Insulin-like growth factor binding proteins in development.

    Silha, Josef V / Murphy, Liam J

    Advances in experimental medicine and biology

    2005  Volume 567, Page(s) 55–89

    Abstract: IGFBPs regulate growth and development by regulating IGF transport to tissues and IGF bioavailability to IGF receptors at cell membrane level. IGFBP excess leads predominantly to inhibition of IGF action and growth retardation with impaired organogenesis. ...

    Abstract IGFBPs regulate growth and development by regulating IGF transport to tissues and IGF bioavailability to IGF receptors at cell membrane level. IGFBP excess leads predominantly to inhibition of IGF action and growth retardation with impaired organogenesis. Absence of human and also mouse ALS leads to decreased IGF-I levels in circulation and causes mild growth retardation. Although IGFBP KO mice demonstrate relatively minor phenotypes, the possibility of compensatory mechanisms that mask the phenotypic manifestation of lack of individual binding proteins needs to be further investigated. Recent studies of hepatic regeneration in IGFBP-1 KO mice and also with mutant IGFBP-3 Tg mice provide some limited support for the existence of IGF-independent mechanism of action in vivo.
    MeSH term(s) Animals ; Embryo, Mammalian/physiology ; Humans ; Insulin-Like Growth Factor Binding Proteins/physiology
    Chemical Substances Insulin-Like Growth Factor Binding Proteins
    Language English
    Publishing date 2005
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/0-387-26274-1_3
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  2. Article: The effects of the insulin-like growth factor-I aptamer, NBI-31772, on glucose homeostasis in the mouse.

    Silha, Josef V / Murphy, Liam J

    Canadian journal of physiology and pharmacology

    2005  Volume 83, Issue 7, Page(s) 557–563

    Abstract: The majority of insulin-like growth factor-I (IGF-I) in the adult rodent circulation is bound to high affinity IGF binding proteins. We investigated the changes in IGF-I clearance, blood glucose and plasma insulin levels, and tissue 2-deoxyglucose uptake ...

    Abstract The majority of insulin-like growth factor-I (IGF-I) in the adult rodent circulation is bound to high affinity IGF binding proteins. We investigated the changes in IGF-I clearance, blood glucose and plasma insulin levels, and tissue 2-deoxyglucose uptake after intravenous administration of the IGF aptamer, NBI-31772, which selectively competes with IGF-I for binding to the IGFBPs, but has no effect at the IGF-I receptor. Clearance of 125I-IGF-I was significantly increased in NBI-31772-treated mice compared with vehicle-treated mice (t1/2 = 45.0 +/- 1.9 vs. 56.3 +/- 3.9 min, respectively; p = 0.021). However, NBI-31772 had no significant effect on glucose levels, and no insulin sparing effect was apparent neither under basal conditions nor during an intravenous glucose challenge. The decline in the specific activity after 3H-2-deoxyglucose administration was significantly less rapid in NBI-31772-treated mice compared with controls, suggesting that the IGF-I aptamer had an inhibitory effect on hepatic gluconeogenesis. In contrast, no insulin-like effect was apparent in other tissues examined. 3H-2-deoxyglucose accumulation was similar in all tissues analyzed, including skeletal muscle, which is thought to be particularly sensitive to IGF-I. These data suggest that the IGF-I aptamer affects clearance of radiolabeled IGF-I from the circulation, but has no marked effects on glucose nor insulin homeostasis. The search for hydrophilic IGF aptamers with longer duration of action that could be used in the treatment of diabetes may be rewarding.
    MeSH term(s) Animals ; Blood Glucose/metabolism ; Catechols/pharmacology ; Deoxyglucose/metabolism ; Glucose/metabolism ; Glucose Tolerance Test ; Homeostasis/drug effects ; Indicators and Reagents ; Insulin/blood ; Insulin-Like Growth Factor Binding Proteins/metabolism ; Insulin-Like Growth Factor I/metabolism ; Insulin-Like Growth Factor I/physiology ; Isoquinolines/pharmacology ; Male ; Mice
    Chemical Substances Blood Glucose ; Catechols ; Indicators and Reagents ; Insulin ; Insulin-Like Growth Factor Binding Proteins ; Isoquinolines ; NBI 31772 ; Insulin-Like Growth Factor I (67763-96-6) ; Deoxyglucose (9G2MP84A8W) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2005-07
    Publishing country Canada
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 127527-6
    ISSN 1205-7541 ; 0008-4212
    ISSN (online) 1205-7541
    ISSN 0008-4212
    DOI 10.1139/y05-041
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  3. Article: Insights from insulin-like growth factor binding protein transgenic mice.

    Silha, Josef V / Murphy, Liam J

    Endocrinology

    2002  Volume 143, Issue 10, Page(s) 3711–3714

    Abstract: The existence of abundant high affinity binding proteins for the IGFs, the IGF binding proteins (IGFBPs), was first demonstrated more than 40 yr ago in the very early days of somatomedin research. With the development of molecular techniques and ... ...

    Abstract The existence of abundant high affinity binding proteins for the IGFs, the IGF binding proteins (IGFBPs), was first demonstrated more than 40 yr ago in the very early days of somatomedin research. With the development of molecular techniques and transgenic and knockout mouse models, the nature, complexity, and redundancy of the IGFBPs have now started to be elucidated. Indeed the functional role of the circulating IGFs and the originally proposed endocrine somatomedin hypothesis have recently been questioned. The limited reports to date indicate that IGFBP knockout mice have few phenotypic manifestations. In contrast, overexpression of IGFBPs in transgenic mice is associated with manifestations that provide some insight into the physiological role of the binding proteins. The predominant effect of generalized or tissue-specific overexpression of the IGFBPs has been growth inhibition as would be anticipated from inhibition of the actions of IGF-I and -II. In addition, impaired glucose homeostasis and reduced fecundity have been observed in both IGFBP-1- and IGFBP-3-overexpressing transgenic mice. This review examines the data reported to date for transgenic mouse models that overexpress IGFBPs. In addition, data from transgenic mice that overexpress the acid-labile subunit, an important component of the ternary complex, have also been reviewed.
    MeSH term(s) Animals ; Carrier Proteins/physiology ; Fertility/physiology ; Glucose/metabolism ; Glycoproteins/physiology ; Homeostasis/physiology ; Humans ; Insulin-Like Growth Factor Binding Proteins/genetics ; Insulin-Like Growth Factor Binding Proteins/physiology ; Mice ; Mice, Transgenic/genetics ; Mice, Transgenic/growth & development ; Mice, Transgenic/physiology
    Chemical Substances Carrier Proteins ; Glycoproteins ; Insulin-Like Growth Factor Binding Proteins ; insulin-like growth factor binding protein, acid labile subunit ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2002-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/en.2002-220116
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  4. Article: Plasma adipokines and body composition in response to modest dietary manipulations in the mouse.

    Silha, Josef V / Weiler, Hope A / Murphy, Liam J

    Obesity (Silver Spring, Md.)

    2006  Volume 14, Issue 8, Page(s) 1320–1329

    Abstract: Objective: The relationship between adipokine levels and body composition has not been carefully examined. Most studies in humans are cross-sectional, and the few studies in mice have been restricted to a comparison of control animals with markedly ... ...

    Abstract Objective: The relationship between adipokine levels and body composition has not been carefully examined. Most studies in humans are cross-sectional, and the few studies in mice have been restricted to a comparison of control animals with markedly obese, insulin-resistant mice. Our objective was to study changes in adipokine levels and body composition in response to modest dietary intervention.
    Research methods and procedures: Plasma resistin, adiponectin, and leptin levels were examined in mice fed ad libitum, a 75% restricted diet, or a diet supplemented with 10% sucrose. Body composition was determined by whole-body DXA.
    Results: The percentage body fat was reduced in mice subjected to the restricted diet and increased in mice supplemented with 10% dextrose. Adipokine levels were not different in either of these groups compared with the control mice. A significant inverse correlation was observed between resistin levels and total body fat, whereas there was no significant correlation between body fat and adiponectin levels. Positive correlations were observed between leptin levels and percentage body fat, total body fat, and abdominal fat. Leptin levels correlated with plasma glucose, but multivariate analysis revealed that this correlation was the result of a strong positive correlation between leptin and insulin levels. There were no correlations between glycemia and resistin or glycemia and adiponectin levels, and no correlation was observed between any of the adipokine levels and bone mineral content or density.
    Discussion: These data suggest that in the mouse, modest dietary perturbations have little effect on resistin and adiponectin levels despite significant effects on glycemia, insulin levels, and bone parameters.
    MeSH term(s) Adiponectin/blood ; Analysis of Variance ; Animals ; Blood Glucose/analysis ; Body Composition/drug effects ; Body Weight/drug effects ; Diet, Reducing ; Dietary Carbohydrates/administration & dosage ; Dietary Supplements ; Insulin/blood ; Leptin/blood ; Male ; Mice ; Peptide Hormones/blood ; Resistin/blood ; Sucrose/administration & dosage
    Chemical Substances Adiponectin ; Blood Glucose ; Dietary Carbohydrates ; Insulin ; Leptin ; Peptide Hormones ; Resistin ; Sucrose (57-50-1)
    Language English
    Publishing date 2006-08
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2230457-5
    ISSN 1930-739X ; 1930-7381 ; 1071-7323
    ISSN (online) 1930-739X
    ISSN 1930-7381 ; 1071-7323
    DOI 10.1038/oby.2006.150
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  5. Article: Sexual dimorphism and regulation of resistin, adiponectin, and leptin expression in the mouse.

    Gui, Yaoting / Silha, Josef V / Murphy, Liam J

    Obesity research

    2004  Volume 12, Issue 9, Page(s) 1481–1491

    Abstract: Objective: To examine gender differences and hormonal regulation of resistin, adiponectin, and leptin.: Research methods and procedures: Plasma levels were measured, and mRNA expression in perigonadal fat was quantified by RNase protection assays.: ...

    Abstract Objective: To examine gender differences and hormonal regulation of resistin, adiponectin, and leptin.
    Research methods and procedures: Plasma levels were measured, and mRNA expression in perigonadal fat was quantified by RNase protection assays.
    Results: Plasma resistin declined with age despite an increase in adiposity in both genders. In male mice, plasma leptin increased, whereas adiponectin levels were constant. In females, both adiponectin and leptin levels increased with age. Resistin mRNA levels were significantly higher in female than male mice at all ages, whereas leptin and adiponectin mRNA levels were similar in fat from 6-week-old male and female mice, and sexual dimorphism was apparent only in the older mice, with higher levels apparent in females. Castration did not abolish gender differences in plasma levels or resistin, adiponectin, or leptin mRNAs. Castration of male mice did not significantly change adipokine mRNA levels or plasma levels of resistin or leptin; however, adiponectin was significantly increased. Dihydrotestosterone treatment had no effect on adipokine mRNA expression or resistin and adiponectin levels but increased leptin levels. In contrast, ovariectomy significantly increased resistin mRNA abundance and decreased leptin and adiponectin mRNAs. Plasma leptin levels were also increased by ovariectomy, whereas resistin and adiponectin levels were unchanged. Estrogen replacement significantly reduced resistin mRNA and increased leptin and adiponectin mRNA levels but had no effect on plasma adipokine levels.
    Discussion: The gender differences in adipokine mRNA expression and plasma levels were not ablated by castration and seem to be dependent on other factors in addition to gonadal steroids.
    MeSH term(s) Adiponectin ; Adipose Tissue/chemistry ; Aging ; Animals ; Female ; Gene Expression Regulation ; Gonads ; Hormones, Ectopic/blood ; Hormones, Ectopic/genetics ; Intercellular Signaling Peptides and Proteins/blood ; Intercellular Signaling Peptides and Proteins/genetics ; Leptin/blood ; Leptin/genetics ; Male ; Mice ; Orchiectomy ; Ovariectomy ; RNA, Messenger/analysis ; Resistin ; Sex Characteristics
    Chemical Substances Adiponectin ; Hormones, Ectopic ; Intercellular Signaling Peptides and Proteins ; Leptin ; RNA, Messenger ; Resistin ; Retn protein, mouse
    Language English
    Publishing date 2004-09
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1201744-9
    ISSN 1550-8528 ; 1071-7323
    ISSN (online) 1550-8528
    ISSN 1071-7323
    DOI 10.1038/oby.2004.185
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  6. Article: Variations in parametrial white adipose tissue mass during the mouse estrous cycle: relationship with the expression of peroxisome proliferator-activated receptor-gamma and retinoic acid receptor-alpha.

    Gui, Yaoting / Cai, Zhiming / Silha, Josef V / Murphy, Liam J

    Canadian journal of physiology and pharmacology

    2006  Volume 84, Issue 8-9, Page(s) 887–892

    Abstract: Estrogen and progestin participate in the regulation of adipose tissue metabolism, and peroxisome proliferator-activated receptor-gamma (PPARgamma) and retinoic acid receptor-alpha (RXRalpha) are absolutely required for adipose tissue development. The ... ...

    Abstract Estrogen and progestin participate in the regulation of adipose tissue metabolism, and peroxisome proliferator-activated receptor-gamma (PPARgamma) and retinoic acid receptor-alpha (RXRalpha) are absolutely required for adipose tissue development. The present study is to investigate the changes in parametrial fat mass and expression of PPARgamma and RXRalpha during estrous cycle in mice. Parametrial white adipose tissues (WAT), inter-scapula brown adipose tissues, and uteri from female mice were weighed. Blood samples were collected for the measurement of 17 beta-estradiol and progesterone levels. An RNase protection assay and Western blot analysis were used to compare the expression of PPARgamma and RXRalpha in adipose tissue. The mass of parametrial WAT in diestrus was significantly higher compared with estrus. However, there is no significant difference on the mass of brown adipose tissues during estrous cycle. The expression of PPARgamma in WAT in diestrus was significantly higher than that in estrus. The expression of RXRalpha during estrous cycle was unchanged in both white and brown adipose tissues. In conclusion, the variation in parametrial WAT mass during the mouse estrous cycle correlates with changes in the expression of PPARgamma in WAT.
    MeSH term(s) Adipose Tissue, Brown/anatomy & histology ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/anatomy & histology ; Adipose Tissue, White/metabolism ; Animals ; Estrous Cycle/metabolism ; Female ; Mice ; Mice, Inbred Strains ; Organ Size ; PPAR gamma/genetics ; PPAR gamma/metabolism ; RNA, Messenger/metabolism ; Receptors, Retinoic Acid/genetics ; Receptors, Retinoic Acid/metabolism ; Retinoic Acid Receptor alpha ; Uterus/anatomy & histology
    Chemical Substances PPAR gamma ; RNA, Messenger ; Rara protein, mouse ; Receptors, Retinoic Acid ; Retinoic Acid Receptor alpha
    Language English
    Publishing date 2006-08
    Publishing country Canada
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 127527-6
    ISSN 1205-7541 ; 0008-4212
    ISSN (online) 1205-7541
    ISSN 0008-4212
    DOI 10.1139/y06-032
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  7. Article: Impaired glucose homeostasis in insulin-like growth factor-binding protein-3-transgenic mice.

    Silha, Josef V / Gui, Yaoting / Murphy, Liam J

    American journal of physiology. Endocrinology and metabolism

    2002  Volume 283, Issue 5, Page(s) E937–45

    Abstract: Glucose homeostasis was examined in male transgenic (Tg) mice that overexpressed the human insulin-like growth factor (IGF)-binding protein (IGFBP)-3 cDNA, driven by either the cytomegalovirus (CMV) or the phosphoglycerate kinase (PGK) promoter. The Tg ... ...

    Abstract Glucose homeostasis was examined in male transgenic (Tg) mice that overexpressed the human insulin-like growth factor (IGF)-binding protein (IGFBP)-3 cDNA, driven by either the cytomegalovirus (CMV) or the phosphoglycerate kinase (PGK) promoter. The Tg mice of both lineages demonstrated increased serum levels of human (h) IGFBP-3 and total IGF-I compared with wild-type (Wt) mice. Fasting blood glucose levels were significantly elevated in 8-wk-old CMV-binding protein (CMVBP)-3- and PGK binding protein (PGKBP)-3-Tg mice compared with Wt mice: 6.35 +/- 0.22 and 5.22 +/- 0.39 vs. 3.99 +/- 0.26 mmol/l, respectively. Plasma insulin was significantly elevated only in CMVBP-3-Tg mice. The responses to a glucose challenge were significantly increased in both Tg strains: area under the glucose curve = 1,824 +/- 65 and 1,910 +/- 115 vs. 1,590 +/- 67 mmol. l(-1). min for CMVBP-3, PGKBP-3, and Wt mice, respectively. The hypoglycemic effects of insulin and IGF-I were significantly attenuated in Tg mice compared with Wt mice. There were no differences in adipose tissue resistin, retinoid X receptor-alpha, or peroxisome proliferator-activated receptor-gamma mRNA levels between Tg and Wt mice. Uptake of 2-deoxyglucose was reduced in muscle and adipose tissue from Tg mice compared with Wt mice. These data demonstrate that overexpression of hIGFBP-3 results in fasting hyperglycemia, impaired glucose tolerance, and insulin resistance.
    MeSH term(s) Animals ; Blood Glucose/metabolism ; Gene Expression/physiology ; Homeostasis/physiology ; Hormones, Ectopic/genetics ; Humans ; Hyperglycemia/genetics ; Insulin Resistance/genetics ; Insulin-Like Growth Factor Binding Protein 3/genetics ; Intercellular Signaling Peptides and Proteins ; Male ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; Nerve Growth Factor ; Proteins ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Retinoic Acid/genetics ; Resistin ; Retinoid X Receptors ; Transcription Factors/genetics
    Chemical Substances Blood Glucose ; Hormones, Ectopic ; Insulin-Like Growth Factor Binding Protein 3 ; Intercellular Signaling Peptides and Proteins ; Proteins ; RETN protein, human ; RETNLB protein, human ; Receptors, Cytoplasmic and Nuclear ; Receptors, Retinoic Acid ; Resistin ; Retinoid X Receptors ; Retn protein, mouse ; Retnla protein, mouse ; Transcription Factors ; Nerve Growth Factor (9061-61-4)
    Language English
    Publishing date 2002-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00014.2002
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  8. Article: Ethnicity, Insulin Resistance, and Inflammatory Adipokines in Women at High and Low Risk for Vascular Disease

    Silha, Josef V / Nyomba, B.L. Grégoire / Leslie, William D / Murphy, Liam J

    Diabetes care. 2007 Feb., v. 30, no. 2

    2007  

    Abstract: OBJECTIVE:--We sought to compare the relationship between body composition, insulin resistance, and inflammatory adipokines in Aboriginal Canadian women, who are at high risk of vascular disease, with white women. RESEARCH DESIGN AND METHODS--A subgroup ... ...

    Abstract OBJECTIVE:--We sought to compare the relationship between body composition, insulin resistance, and inflammatory adipokines in Aboriginal Canadian women, who are at high risk of vascular disease, with white women. RESEARCH DESIGN AND METHODS--A subgroup of the First Nations Bone Health Study population, consisting of 131 Aboriginal women and 132 matched white women, was utilized. Body composition was determined by whole-body dual X-ray absorptiometry, and blood analytes were measured after an overnight fast. RESULTS:--After excluding individuals with diabetes, A1C, BMI, percent trunk fat, and homeostasis model assessment of insulin resistance (HOMA-IR) were greater in First Nation women compared with white women, whereas adiponectin, retinol binding protein (RBP)4, and insulin-like growth factor binding protein-1 (IGFBP-1) were lower. First Nation women had more trunk fat for any given level of total fat than white women. There were no differences in resistin, leptin, tumor necrosis factor (TNF)-α, or C-reactive protein (CRP) levels between First Nation and white women. Insulin resistance correlated with leptin and inversely with adiponectin levels in both First Nation and white women. There were weak correlations between insulin resistance and TNF-α, interleukin-6, and CRP, but these were not significant after correction for body fat. No correlation was found between RBP4 and insulin resistance. ANCOVA revealed a higher HOMA-IR adjusted for total body fat in First Nation women than in white women (P = 0.015) but not HOMA-IR adjusted for trunk fat (P > 0.2). CONCLUSIONS:--First Nation women are more insulin resistant than white women, and this is explained by trunk fat but not total fat. Despite the increased insulin resistance, inflammatory adipokines are not significantly increased in First Nation women compared with white women.
    Keywords C-reactive protein ; Canadians ; First Nations ; Whites ; X-radiation ; adiponectin ; blood ; body fat ; body mass index ; diabetes ; homeostasis ; insulin ; insulin resistance ; interleukin-6 ; leptin ; resistin ; retinol-binding protein ; risk ; tumor necrosis factor-alpha ; women
    Language English
    Size p. 286-291.
    Publishing place American Diabetes Association
    Document type Article
    ZDB-ID 441231-x
    ISSN 1935-5548 ; 0149-5992
    ISSN (online) 1935-5548
    ISSN 0149-5992
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  9. Article: Ethnicity, insulin resistance, and inflammatory adipokines in women at high and low risk for vascular disease.

    Silha, Josef V / Nyomba, B L Grégoire / Leslie, William D / Murphy, Liam J

    Diabetes care

    2007  Volume 30, Issue 2, Page(s) 286–291

    Abstract: Objective: We sought to compare the relationship between body composition, insulin resistance, and inflammatory adipokines in Aboriginal Canadian women, who are at high risk of vascular disease, with white women.: Research design and methods: A ... ...

    Abstract Objective: We sought to compare the relationship between body composition, insulin resistance, and inflammatory adipokines in Aboriginal Canadian women, who are at high risk of vascular disease, with white women.
    Research design and methods: A subgroup of the First Nations Bone Health Study population, consisting of 131 Aboriginal women and 132 matched white women, was utilized. Body composition was determined by whole-body dual X-ray absorptiometry, and blood analytes were measured after an overnight fast.
    Results: After excluding individuals with diabetes, A1C, BMI, percent trunk fat, and homeostasis model assessment of insulin resistance (HOMA-IR) were greater in First Nation women compared with white women, whereas adiponectin, retinol binding protein (RBP)4, and insulin-like growth factor binding protein-1 (IGFBP-1) were lower. First Nation women had more trunk fat for any given level of total fat than white women. There were no differences in resistin, leptin, tumor necrosis factor (TNF)-alpha, or C-reactive protein (CRP) levels between First Nation and white women. Insulin resistance correlated with leptin and inversely with adiponectin levels in both First Nation and white women. There were weak correlations between insulin resistance and TNF-alpha, interleukin-6, and CRP, but these were not significant after correction for body fat. No correlation was found between RBP4 and insulin resistance. ANCOVA revealed a higher HOMA-IR adjusted for total body fat in First Nation women than in white women (P = 0.015) but not HOMA-IR adjusted for trunk fat (P > 0.2).
    Conclusions: First Nation women are more insulin resistant than white women, and this is explained by trunk fat but not total fat. Despite the increased insulin resistance, inflammatory adipokines are not significantly increased in First Nation women compared with white women.
    MeSH term(s) Adiponectin/blood ; Adult ; Blood Glucose/metabolism ; Body Composition ; Body Mass Index ; Ethnic Groups ; European Continental Ancestry Group ; Female ; Humans ; Indians, North American ; Inflammation/blood ; Inflammation/physiopathology ; Insulin/blood ; Insulin Resistance ; Manitoba ; Middle Aged ; Risk Factors ; Vascular Diseases/epidemiology
    Chemical Substances Adiponectin ; Blood Glucose ; Insulin
    Language English
    Publishing date 2007-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 441231-x
    ISSN 1935-5548 ; 0149-5992
    ISSN (online) 1935-5548
    ISSN 0149-5992
    DOI 10.2337/dc06-1073
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  10. Article: Plasma Adipokines and Body Composition in Response to Modest Dietary Manipulations in the Mouse

    Silha, Josef V / Weiler, Hope A / Murphy, Liam J

    Obesity research. 2006 Aug., v. 14, no. 8

    2006  

    Abstract: OBJECTIVE: The relationship between adipokine levels and body composition has not been carefully examined. Most studies in humans are cross-sectional, and the few studies in mice have been restricted to a comparison of control animals with markedly obese, ...

    Abstract OBJECTIVE: The relationship between adipokine levels and body composition has not been carefully examined. Most studies in humans are cross-sectional, and the few studies in mice have been restricted to a comparison of control animals with markedly obese, insulin-resistant mice. Our objective was to study changes in adipokine levels and body composition in response to modest dietary intervention. RESEARCH METHODS AND PROCEDURES: Plasma resistin, adiponectin, and leptin levels were examined in mice fed ad libitum, a 75% restricted diet, or a diet supplemented with 10% sucrose. Body composition was determined by whole-body DXA. RESULTS: The percentage body fat was reduced in mice subjected to the restricted diet and increased in mice supplemented with 10% dextrose. Adipokine levels were not different in either of these groups compared with the control mice. A significant inverse correlation was observed between resistin levels and total body fat, whereas there was no significant correlation between body fat and adiponectin levels. Positive correlations were observed between leptin levels and percentage body fat, total body fat, and abdominal fat. Leptin levels correlated with plasma glucose, but multivariate analysis revealed that this correlation was the result of a strong positive correlation between leptin and insulin levels. There were no correlations between glycemia and resistin or glycemia and adiponectin levels, and no correlation was observed between any of the adipokine levels and bone mineral content or density. DISCUSSION: These data suggest that in the mouse, modest dietary perturbations have little effect on resistin and adiponectin levels despite significant effects on glycemia, insulin levels, and bone parameters.
    Keywords mice ; animal disease models ; obesity ; metabolic syndrome ; overweight ; nutritional intervention ; restricted feeding ; ad libitum feeding ; high carbohydrate diet ; sucrose ; hormone secretion ; body fat ; dual-energy X-ray absorptiometry ; bone mineralization ; bone density ; fat free mass ; leptin ; resistin
    Language English
    Dates of publication 2006-08
    Size p. 1320-1329.
    Publishing place The North American Association for the Study of Obesity
    Document type Article
    ZDB-ID 1201744-9
    ISSN 1550-8528 ; 1071-7323
    ISSN (online) 1550-8528
    ISSN 1071-7323
    Database NAL-Catalogue (AGRICOLA)

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