Galectin-3 Deficiency Accelerates High-Fat Diet–Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets

Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet–induced obesity and diabetes. Obese LGALS3−/− mice have increased body weig...

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Bibliographische Detailangaben
Veröffentlicht in:Diabetes (New York, N.Y.) Jg. 62; H. 6; S. 1932 - 1944
Hauptverfasser: Pejnovic, Nada N., Pantic, Jelena M., Jovanovic, Ivan P., Radosavljevic, Gordana D., Milovanovic, Marija Z., Nikolic, Ivana G., Zdravkovic, Nemanja S., Djukic, Aleksandar L., Arsenijevic, Nebojsa N., Lukic, Miodrag L.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Alexandria, VA American Diabetes Association 01.06.2013
Schlagworte:
Ablation
Adipose Tissue - immunology
Adipose Tissue - metabolism
Age
Analysis
Animals
Antibodies
Biological and medical sciences
Blotting, Western
Body fat
Body Weight - genetics
Body Weight - physiology
Cells, Cultured
Cytokines
Diabetes
Diabetes. Impaired glucose tolerance
Diet
Diet, High-Fat - adverse effects
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Flow Cytometry
Galectin 3 - deficiency
Galectin 3 - genetics
Glucose
Homeostasis
Immunohistochemistry
Inflammation
Inflammation - genetics
Inflammation - metabolism
Insulin resistance
Islets of Langerhans - immunology
Islets of Langerhans - metabolism
Lectins
Medical sciences
Metabolic diseases
Metabolism
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Obesity
Obesity - etiology
Obesity - immunology
Obesity - metabolism
Original Research
RNA, Small Interfering
Endocrinopathy
Obesity
Adipose tissue
Diet
Diabetes mellitus
Deficiency
Nutrition disorder
Inflammation
Pancreas
Nutritional status
Feeding
ISSN:0012-1797, 1939-327X, 1939-327X
Online-Zugang:Volltext
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Abstract Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet–induced obesity and diabetes. Obese LGALS3−/− mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3−/− mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c+CD11b+ macrophages and decreased CD4+CD25+FoxP3+ regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1β (IL-1β) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3−/− animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3−/− peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1–dependent IL-1β production and increased phosphorylation of NF-κB p65 compared with WT cells. Transfection of LGALS3−/− macrophages with NLRP3 small interfering RNA attenuated IL-1β production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
AbstractList Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese LGALS3(-/-) mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3(-/-) mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c(+)CD11b(+) macrophages and decreased CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1[beta] (IL-1[beta]) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3(-/-) animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1-dependent IL-1[beta] production and increased phosphorylation of NF-κB p65 compared with WT cells. Transfection of LGALS3(-/-) macrophages with NLRP3 small interfering RNA attenuated IL-1[beta] production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese [LGALS3.sup.-/-] mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese [LGALS3.sup.-/-] mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory [CD11c.sup.+][CD11b.sup.+] macrophages and decreased [CD4.sup.+][CD25.sup.+][FoxP3.sup.+] regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1[beta] (IL-1[beta]) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese [LGALS3.sup.-/-] animals accompanied with elevated phosphorylated nuclear factor-[kappa]B (NF-[kappa]B) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of [LGALS3.sup.-/-] peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1-dependent IL-1[beta] production and increased phosphorylation of NF-[kappa]B p65 compared with WT cells. Transfection of [LGALS3.sup.-/-] macrophages with NLRP3 small interfering RNA attenuated IL-1[beta] production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet–induced obesity and diabetes. Obese LGALS3−/− mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3−/− mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c+CD11b+ macrophages and decreased CD4+CD25+FoxP3+ regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1β (IL-1β) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3−/− animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3−/− peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1–dependent IL-1β production and increased phosphorylation of NF-κB p65 compared with WT cells. Transfection of LGALS3−/− macrophages with NLRP3 small interfering RNA attenuated IL-1β production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese LGALS3(-/-) mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3(-/-) mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c(+)CD11b(+) macrophages and decreased CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1β (IL-1β) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3(-/-) animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1-dependent IL-1β production and increased phosphorylation of NF-κB p65 compared with WT cells. Transfection of LGALS3(-/-) macrophages with NLRP3 small interfering RNA attenuated IL-1β production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese LGALS3(-/-) mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3(-/-) mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c(+)CD11b(+) macrophages and decreased CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1β (IL-1β) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3(-/-) animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1-dependent IL-1β production and increased phosphorylation of NF-κB p65 compared with WT cells. Transfection of LGALS3(-/-) macrophages with NLRP3 small interfering RNA attenuated IL-1β production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese [LGALS3.sup.-/-] mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese [LGALS3.sup.-/-] mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory [CD11c.sup.+][CD11b.sup.+] macrophages and decreased [CD4.sup.+][CD25.sup.+][FoxP3.sup.+] regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1β (IL-1β) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese [LGALS3.sup.-/-] animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of [LGALS3.sup.-/-] peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1-dependent IL-1β production and increased phosphorylation of NF-κB p65 compared with WT cells. Transfection of [LGALS3.sup.-/-] macrophages with NLRP3 small interfering RNA attenuated IL-1β production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3 (Gal-3), a galactoside-binding lectin, accelerates high-fat diet-induced obesity and diabetes. Obese LGALS3(-/-) mice have increased body weight, amount of total visceral adipose tissue (VAT), fasting blood glucose and insulin levels, homeostasis model assessment of insulin resistance, and markers of systemic inflammation compared with diet-matched wild-type (WT) animals. VAT of obese LGALS3(-/-) mice exhibited increased incidence of type 1 T and NKT lymphocytes and proinflammatory CD11c(+)CD11b(+) macrophages and decreased CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages. Pronounced mononuclear cell infiltrate, increased expression of NLRP3 inflammasome and interleukin-1β (IL-1β) in macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancreatic islets of obese LGALS3(-/-) animals accompanied with elevated phosphorylated nuclear factor-κB (NF-κB) p65 and mature caspase-1 protein expression in pancreatic tissue and VAT. In vitro stimulation of LGALS3(-/-) peritoneal macrophages with lipopolysaccharide (LPS) and saturated fatty acid palmitate caused increased caspase-1-dependent IL-1β production and increased phosphorylation of NF-κB p65 compared with WT cells. Transfection of LGALS3(-/-) macrophages with NLRP3 small interfering RNA attenuated IL-1β production in response to palmitate and LPS plus palmitate. Obtained results suggest important protective roles for Gal-3 in obesity-induced inflammation and diabetes.
Audience Professional
Author Djukic, Aleksandar L.
Pejnovic, Nada N.
Lukic, Miodrag L.
Milovanovic, Marija Z.
Arsenijevic, Nebojsa N.
Nikolic, Ivana G.
Pantic, Jelena M.
Jovanovic, Ivan P.
Radosavljevic, Gordana D.
Zdravkovic, Nemanja S.
Author_xml – sequence: 1
  givenname: Nada N.
  surname: Pejnovic
  fullname: Pejnovic, Nada N.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia, Institute of Pathophysiology, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia
– sequence: 2
  givenname: Jelena M.
  surname: Pantic
  fullname: Pantic, Jelena M.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia
– sequence: 3
  givenname: Ivan P.
  surname: Jovanovic
  fullname: Jovanovic, Ivan P.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia
– sequence: 4
  givenname: Gordana D.
  surname: Radosavljevic
  fullname: Radosavljevic, Gordana D.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia
– sequence: 5
  givenname: Marija Z.
  surname: Milovanovic
  fullname: Milovanovic, Marija Z.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia
– sequence: 6
  givenname: Ivana G.
  surname: Nikolic
  fullname: Nikolic, Ivana G.
  organization: Department of Immunology, Institute for Biological Research “Sinisa Stankovic,” University of Belgrade, Belgrade, Serbia
– sequence: 7
  givenname: Nemanja S.
  surname: Zdravkovic
  fullname: Zdravkovic, Nemanja S.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia
– sequence: 8
  givenname: Aleksandar L.
  surname: Djukic
  fullname: Djukic, Aleksandar L.
  organization: Institute of Pathophysiology, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia, Center for Endocrinology, Diabetes, and Metabolic Diseases, Clinical Center Kragujevac, Kragujevac, Serbia
– sequence: 9
  givenname: Nebojsa N.
  surname: Arsenijevic
  fullname: Arsenijevic, Nebojsa N.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia
– sequence: 10
  givenname: Miodrag L.
  surname: Lukic
  fullname: Lukic, Miodrag L.
  organization: Center for Molecular Medicine and Stem Cell Research, Kragujevac, Serbia
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27485202$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/23349493$$D View this record in MEDLINE/PubMed
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10.1161/ATVBAHA.109.186791
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10.1111/j.1365-2567.2007.02724.x
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Issue 6
Keywords Endocrinopathy
Obesity
Adipose tissue
Diet
Diabetes mellitus
Deficiency
Nutrition disorder
Inflammation
Pancreas
Nutritional status
Feeding
Language English
License CC BY 4.0
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
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N.N.P. and J.M.P. contributed equally to this study.
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PublicationTitle Diabetes (New York, N.Y.)
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Snippet Obesity-induced diabetes is associated with low-grade inflammation in adipose tissue and macrophage infiltration of islets. We show that ablation of galectin-3...
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SourceType Open Access Repository
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StartPage 1932
SubjectTerms Ablation
Adipose Tissue - immunology
Adipose Tissue - metabolism
Age
Analysis
Animals
Antibodies
Biological and medical sciences
Blotting, Western
Body fat
Body Weight - genetics
Body Weight - physiology
Cells, Cultured
Cytokines
Diabetes
Diabetes. Impaired glucose tolerance
Diet
Diet, High-Fat - adverse effects
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Flow Cytometry
Galectin 3 - deficiency
Galectin 3 - genetics
Glucose
Homeostasis
Immunohistochemistry
Inflammation
Inflammation - genetics
Inflammation - metabolism
Insulin resistance
Islets of Langerhans - immunology
Islets of Langerhans - metabolism
Lectins
Medical sciences
Metabolic diseases
Metabolism
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Obesity
Obesity - etiology
Obesity - immunology
Obesity - metabolism
Original Research
RNA, Small Interfering
Title Galectin-3 Deficiency Accelerates High-Fat Diet–Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets
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Volume 62
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