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il-interleukin

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Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(7):1106–1115
Published: 01 July 2000
... evaluated for intrinsically dysregulated cytokine production with the potential to initiate or exacerbate disease. Endotoxin-activated peritoneal Mø from young prediseased NOD mice produced interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha levels similar to those of Mø from a panel of control strains...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(9):1730–1736
Published: 01 September 1999
...N Giannoukakis; W A Rudert; S C Ghivizzani; A Gambotto; C Ricordi; M Trucco; P D Robbins The beta-cells in the pancreatic islets of Langerhans are the targets of autoreactive T-cells and are destroyed in type 1 diabetes. Macrophage-derived interleukin-1beta (IL-1beta) is important in eliciting beta...
Meeting Abstracts
Journal: Diabetes
Diabetes 2020;69(Supplement_1):278-OR
Published: 01 June 2020
...MATTHIAS G. VON HERRATH; STEPHEN C. BAIN; BRUCE W. BODE; JESPER OLE CLAUSEN; KEN COPPIETERS; LEYLYA GAYSINA; JANUSZ GUMPRECHT; TROELS K. HANSEN; CHANTAL MATHIEU; CRISTOBAL MORALES PORTILLO; OFRI MOSENZON; STINE SEGEL; GEORGE M. TSOUKAS; THOMAS PIEBER Objective: To evaluate the effect of anti-IL-21...
Meeting Abstracts
Journal: Diabetes
Diabetes 2020;69(Supplement_1):1887-P
Published: 01 June 2020
... for 24 h, measured mRNA levels by real-time reverse transcription polymerase chain reaction, and found that IH significantly increased the mRNA levels of interleukin-8 (IL-8), osteonectin (ON), and myonectin (MN). IL-8, ON, and MN in IH-treated RD cell medium were also...
Journal Articles
Journal: Diabetes
Diabetes 2011;60(6):1688–1698
Published: 21 May 2011
... of interleukin-1 receptor I (IL-1RI)-mediated signals to this phenotype has not been defined. We hypothesized that lack of IL-1RI may ameliorate HFD-induced IR by attenuating adipose tissue inflammation. RESEARCH DESIGN AND METHODS Glucose homeostasis was monitored in chow- and HFD-fed wild-type (WT) and IL...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 1984;33(6):552–555
Published: 01 June 1984
...Karen S Zier; Martha M Leo; Richard S Spielman; Lester Baker Synthesis of interleukin-2 (IL-2) by lymphocytes from 26 insulin-dependent diabetic subjects (IDDM) was compared with that by lymphocytes from 24 nondiabetic control subjects. The control group produced 1.001 ± 0.071 U/ml (mean ± SEM...
Images
Increased adipose tissue inflammation in ASKO mice. Mac2 immunostaining in ...
Published: 14 June 2014
Figure 5 Increased adipose tissue inflammation in ASKO mice. Mac2 immunostaining in Epi-WAT (A) and BAT (B) from 3-, 6-, and 10-month-old WT and ASKO mice, with arrows indicating crown-like structures. M, month. Scale bar is 50 μm. Relative mRNA levels of macrophage markers and inflammatory cytokines in Epi-WAT (n = 5) (C) and BAT (n = 7) (D) from 6- and 10-month-old WT and ASKO mice. IL, interleukin; TGF, transforming growth factor. Values are expressed as mean ± SEM. *P < 0.05, **P < 0.01 for ASKO vs. WT. Figure 5. Increased adipose tissue inflammation in ASKO mice. Mac2 immunostaining in Epi-WAT (A) and BAT (B) from 3-, 6-, and 10-month-old WT and ASKO mice, with arrows indicating crown-like structures. M, month. Scale bar is 50 μm. Relative mRNA levels of macrophage markers and inflammatory cytokines in Epi-WAT (n = 5) (C) and BAT (n = 7) (D) from 6- and 10-month-old WT and ASKO mice. IL, interleukin; TGF, transforming growth factor. Values are expressed as mean ± SEM. *P < 0.05, **P < 0.01 for ASKO vs. WT. More
Images
No effect on insulin-reactive 4-8 T-cell development in Ins<sup>Y16A</sup> ...
Published: 13 December 2020
Figure 3 No effect on insulin-reactive 4-8 T-cell development in InsY16A mutant mice. Sublethally irradiated 8- to 12-week-old female CD45.1 NOD or NOD.Y16A mice were reconstituted with insulin-reactive 4-8 TCR Rg CD45.2 NOD.scid bone marrow from 7- to 9-week-old mice (n = 5 mice/group). Black circles, WT; red circles, Y16A. A: Schematic diagram for the generation of TCR Rg mice (top) and CD45.2+ thymic cellularity (bottom). B: CD4SP ratio and number, TCR MFI, and CD5 MFI were determined in CD45.2+ thymocytes. C: CD4+TCR+CD45.2+ 4-8 T-cell numbers in spleens and islets. Statistical analysis was performed using a Mann-Whitney nonparametric test; error bars designate mean ± SD. **P < 0.01. IL, interleukin; SCF, stem cell factor. Figure 3. No effect on insulin-reactive 4-8 T-cell development in InsY16A mutant mice. Sublethally irradiated 8- to 12-week-old female CD45.1 NOD or NOD.Y16A mice were reconstituted with insulin-reactive 4-8 TCR Rg CD45.2 NOD.scid bone marrow from 7- to 9-week-old mice (n = 5 mice/group). Black circles, WT; red circles, Y16A. A: Schematic diagram for the generation of TCR Rg mice (top) and CD45.2+ thymic cellularity (bottom). B: CD4SP ratio and number, TCR MFI, and CD5 MFI were determined in CD45.2+ thymocytes. C: CD4+TCR+CD45.2+ 4-8 T-cell numbers in spleens and islets. Statistical analysis was performed using a Mann-Whitney nonparametric test; error bars designate mean ± SD. **P < 0.01. IL, interleukin; SCF, stem cell factor. More
Images
Fructose induces hepatotoxicity and massive liver glycogen accumulation in ...
Published: 23 January 2020
Figure 2 Fructose induces hepatotoxicity and massive liver glycogen accumulation in ChLO mice. A: Body weight in control and ChLO groups. B: Blood glucose levels in the fed or 6-h-fasted states. C: Plasma TG and cholesterol levels in the fed state. D: Plasma transaminases levels. E: Liver weight/body weight ratios. F: Morphological changes demonstrated by H-E staining and PAS staining for glycogen (pink). Scale bar, 100 μm. G: Glycogen contents in the liver and muscle in the fed state. H: Correlation between liver glycogen contents and plasma ALT levels. I: Liver TG and cholesterol contents. J: mRNA expression of the inflammatory factors in the liver. K: mRNA level of genes involved in ER stress in the liver. L: Western blot analysis for ATF6 expression and activation. n = 5–12. *P < 0.05; **P < 0.01. IL, interleukin; PAS, periodic acid Schiff; TC, total cholesterol. Figure 2. Fructose induces hepatotoxicity and massive liver glycogen accumulation in ChLO mice. A: Body weight in control and ChLO groups. B: Blood glucose levels in the fed or 6-h-fasted states. C: Plasma TG and cholesterol levels in the fed state. D: Plasma transaminases levels. E: Liver weight/body weight ratios. F: Morphological changes demonstrated by H-E staining and PAS staining for glycogen (pink). Scale bar, 100 μm. G: Glycogen contents in the liver and muscle in the fed state. H: Correlation between liver glycogen contents and plasma ALT levels. I: Liver TG and cholesterol contents. J: mRNA expression of the inflammatory factors in the liver. K: mRNA level of genes involved in ER stress in the liver. L: Western blot analysis for ATF6 expression and activation. n = 5–12. *P < 0.05; **P < 0.01. IL, interleukin; PAS, periodic acid Schiff; TC, total cholesterol. More
Images
PLIN5 overexpression in muscle protects the liver in mice fed an HF diet. ...
Published: 31 March 2015
Figure 4 PLIN5 overexpression in muscle protects the liver in mice fed an HF diet. A: Weights of mice on an HF diet. Mice were weighed weekly for 9 weeks (NTG mice, n = 17; MCK-Plin5 mice, n = 14). B: Lean and fat mass as a percentage of body weight (NTG mice, n = 4; MCK-Plin5 mice, n = 7). C: Glucose tolerance. D: Insulin sensitivity. The data shown are representative of two separate experiments. E: Liver weights, liver cholesterol, NEFA, and TAG. Liver weight is expressed as a percentage of body weight (BW), and lipid content is normalized to milligrams protein. F: Quantitative RT-PCR data showing gene expression of lipid transport and metabolism genes (left) and markers of inflammation in the livers of mice fed an HF diet (right) (NTG mice, n = 10; MCK-Plin5 mice, n = 9). *P < 0.05; **P < 0.01. IL, interleukin; n.s., not significant; TNF, tumor necrosis factor. Figure 4. PLIN5 overexpression in muscle protects the liver in mice fed an HF diet. A: Weights of mice on an HF diet. Mice were weighed weekly for 9 weeks (NTG mice, n = 17; MCK-Plin5 mice, n = 14). B: Lean and fat mass as a percentage of body weight (NTG mice, n = 4; MCK-Plin5 mice, n = 7). C: Glucose tolerance. D: Insulin sensitivity. The data shown are representative of two separate experiments. E: Liver weights, liver cholesterol, NEFA, and TAG. Liver weight is expressed as a percentage of body weight (BW), and lipid content is normalized to milligrams protein. F: Quantitative RT-PCR data showing gene expression of lipid transport and metabolism genes (left) and markers of inflammation in the livers of mice fed an HF diet (right) (NTG mice, n = 10; MCK-Plin5 mice, n = 9). *P < 0.05; **P < 0.01. IL, interleukin; n.s., not significant; TNF, tumor necrosis factor. More
Images
The placenta may play a role in the intrauterine origin of adult metabolic ...
Published: 07 January 2021
Figure 1 The placenta may play a role in the intrauterine origin of adult metabolic disease through several mechanisms, such as by determining the flux of oxygen, nutrients, and methyl donors to the fetus, thereby regulating fetal growth and development. The activity of placental insulin/IGF-1 sig... More
Images
Clinical correlates of HSPC levels in COVID-19. <em>A</em>: The str...
Published: 21 January 2022
Figure 2 Clinical correlates of HSPC levels in COVID-19. A: The strongest correlations for CD34+ HSPCs are shown as scatter plots. Patients are divided according to good or poor outcome (admittance to the ICU or death) using the color code described in the legend. Pearson r coefficients and the respective P values are shown. B: The heat map shows values of the Pearson r coefficients for each antigenic definition of HSPCs and their relative and absolute cell count in peripheral blood. The code color allows easy interpretation: intense blue represents strong direct correlation, intense red represents strong inverse correlation, and white represents no correlation. Cell boxing indicates statistical significance at P < 0.05. ARB, angiotensin receptor blocker; CCB, calcium channel blocker; COPD, chronic obstructive pulmonary disease; CRP, C-reactive protein; IL, interleukin; LDH, lactate dehydrogenase; WBC, white blood count. More
Images
Expression and activity of <em>IκBα/I</em>κBα<em>M</em> in ...
Published: 01 January 2005
FIG. 2. Expression and activity of IκBα/IκBαM in adult pancreatic islet cells. A and B: Immunohistological analyses using anti-IκBα antibodies show that IκBα is highly expressed in α-cells in adult pancreas and at lower levels in the centrally located β-cells (A). WT, wild type. B: In NIβ islets, an increased, high level of IκBα/IκBαM expression is observed in β-cells. C: Western blot analysis of islets isolated from wild-type (wt) and two independent transgenic lines (A and C) showing expression of both the endogenous IκBα and the mutant IκBαM. D: Correlation between transgene copy number and expression levels normalized to endogenous IκBα levels. E: In vitro expression of IκBαM and cytokine induced NF-κB–regulated genes by real-time PCR. Cytokine-stimulated NIβ islets express significantly reduced levels of iNOS, MnSOD, and Iκβα compared with wild-type islets. Cytokine-stimulated NIβ islets express 4.4% IκBαM compared with freshly isolated NIβ islets (n = 3). Data are average values ± SE. IL, interleukin; INF, interferon. *P < 0.05; **P < 0.01. FIG. 2. Expression and activity of IκBα/IκBαM in adult pancreatic islet cells. A and B: Immunohistological analyses using anti-IκBα antibodies show that IκBα is highly expressed in α-cells in adult pancreas and at lower levels in the centrally located β-cells (A). WT, wild type. B: In NIβ islets, an increased, high level of IκBα/IκBαM expression is observed in β-cells. C: Western blot analysis of islets isolated from wild-type (wt) and two independent transgenic lines (A and C) showing expression of both the endogenous IκBα and the mutant IκBαM. D: Correlation between transgene copy number and expression levels normalized to endogenous IκBα levels. E: In vitro expression of IκBαM and cytokine induced NF-κB–regulated genes by real-time PCR. Cytokine-stimulated NIβ islets express significantly reduced levels of iNOS, MnSOD, and Iκβα compared with wild-type islets. Cytokine-stimulated NIβ islets express 4.4% IκBαM compared with freshly isolated NIβ islets (n = 3). Data are average values ± SE. IL, interleukin; INF, interferon. *P < 0.05; **P < 0.01. More
Images
Characterization of adipose tissue–specific SNRK knockout (SNRK<sup>fat−/−,</sup>...
Published: 03 January 2018
Figure 4 Characterization of adipose tissue–specific SNRK knockout (SNRKfat−/−, A-Cre) and littermate control (SNRKloxp/loxp, SNRKA-Cre) mice. A: SNRK gene expression in WAT of SNRKloxp/loxp, SNRKfat−/−, A-Cre, and SNRKA-Cre mice (n = 3 or 4 mice/per group). B: Histology of the subcutaneous WAT depot stained with hematoxylin-eosin (HE; upper panels) or F4/80 antibody (lower panels). C: Expression of cytokine and chemokine genes in primary adipocytes isolated from SNRKfat−/−, A-Cre and littermate control mice (n = 7–12 mice/group). D: Expression of F4/80, CD11c, and ATG12 genes in gonadal WAT from SNRKfat−/−, A-Cre and littermate control mice (n = 4 mice/group). E: Plasma cytokine and chemokine levels in SNRKfat−/−, A-Cre and littermate control mice (n = 7–12 mice/group). F: Glucose tolerance test results from SNRKfat−/−, A-Cre mice and littermate control mice fed a chow diet (n = 7–12 mice/group). G: Insulin tolerance test results from SNRKfat−/−, A-Cre mice (n = 8 mice/group) and littermate control mice fed (n = 5–9 mice/group) fed an HFD for 20 weeks. *P < 0.05, SNRKfat−/−, A-Cre vs. SNRKloxp/loxp; #P < 0.05, SNRKfat−/−, A-Cre vs. SNRKA-Cre. IL, interleukin. Figure 4. Characterization of adipose tissue–specific SNRK knockout (SNRKfat−/−, A-Cre) and littermate control (SNRKloxp/loxp, SNRKA-Cre) mice. A: SNRK gene expression in WAT of SNRKloxp/loxp, SNRKfat−/−, A-Cre, and SNRKA-Cre mice (n = 3 or 4 mice/per group). B: Histology of the subcutaneous WAT depot stained with hematoxylin-eosin (HE; upper panels) or F4/80 antibody (lower panels). C: Expression of cytokine and chemokine genes in primary adipocytes isolated from SNRKfat−/−, A-Cre and littermate control mice (n = 7–12 mice/group). D: Expression of F4/80, CD11c, and ATG12 genes in gonadal WAT from SNRKfat−/−, A-Cre and littermate control mice (n = 4 mice/group). E: Plasma cytokine and chemokine levels in SNRKfat−/−, A-Cre and littermate control mice (n = 7–12 mice/group). F: Glucose tolerance test results from SNRKfat−/−, A-Cre mice and littermate control mice fed a chow diet (n = 7–12 mice/group). G: Insulin tolerance test results from SNRKfat−/−, A-Cre mice (n = 8 mice/group) and littermate control mice fed (n = 5–9 mice/group) fed an HFD for 20 weeks. *P < 0.05, SNRKfat−/−, A-Cre vs. SNRKloxp/loxp; #P < 0.05, SNRKfat−/−, A-Cre vs. SNRKA-Cre. IL, interleukin. More
Images
BAT-MACT in vivo characteristics. <em>A</em>: Persistence of BAT-MA...
Published: 20 August 2015
Figure 3 BAT-MACT in vivo characteristics. A: Persistence of BAT-MACT over time monitored by luciferase activity in live animals (FVB/NJ; n = 5); false color heat scale image indicating average (Avg) photon radiance. Max, maximum; Min, minimum; sr, steradian. B: Macroscopic morphology of implants after 2 weeks. BAT-MACTs were removed after 14 days; fixed, cryosectioned, and stained with DAPI; and stained for the vascularization marker endomucin (C) or neutral lipids (green) and UCP1 (red) (D). E: mRNA expression of UCP1 relative to WAT using samples from differentiated ADMSCs plated on Ag73 and C16 peptide-coated TCPS or in Ag73- and C16-conjugated AcHyA hydrogels cultured in vitro or implanted into recipient animals (FVB/NJ; n = 4, 3, or 6, respectively). F: PRDM16 and PPARγ mRNA expression normalized to GAPDH of BAT-MACTs after 2 weeks in vivo relative to endogenous BAT (FVB/NJ; n = 9). G: UCP1 protein expression of BAT-MACTs generated with ADMSCs from visceral or subcutaneous FVB/NJ or C57BL/6J mice 2 weeks postimplantation into a syngenic recipient relative to endogenous BAT (n = 3). NS, not significant. H: UCP1 protein expressed in BAT-MACTs of different implant sites after 2 weeks in vivo relative to endogenous BAT (FVB/NJ; n = 5). I: Serum cytokine levels measured 2 weeks postimplantation of BAT-MACT or the same ADMSCs delivered via PBS. Animals were administered the 60% fat diet for the duration of this study (C57BL/6J; n = 6). IL, interleukin. Significance at **P < 0.01 and ***P < 0.001. Figure 3. BAT-MACT in vivo characteristics. A: Persistence of BAT-MACT over time monitored by luciferase activity in live animals (FVB/NJ; n = 5); false color heat scale image indicating average (Avg) photon radiance. Max, maximum; Min, minimum; sr, steradian. B: Macroscopic morphology of implants after 2 weeks. BAT-MACTs were removed after 14 days; fixed, cryosectioned, and stained with DAPI; and stained for the vascularization marker endomucin (C) or neutral lipids (green) and UCP1 (red) (D). E: mRNA expression of UCP1 relative to WAT using samples from differentiated ADMSCs plated on Ag73 and C16 peptide-coated TCPS or in Ag73- and C16-conjugated AcHyA hydrogels cultured in vitro or implanted into recipient animals (FVB/NJ; n = 4, 3, or 6, respectively). F: PRDM16 and PPARγ mRNA expression normalized to GAPDH of BAT-MACTs after 2 weeks in vivo relative to endogenous BAT (FVB/NJ; n = 9). G: UCP1 protein expression of BAT-MACTs generated with ADMSCs from visceral or subcutaneous FVB/NJ or C57BL/6J mice 2 weeks postimplantation into a syngenic recipient relative to endogenous BAT (n = 3). NS, not significant. H: UCP1 protein expressed in BAT-MACTs of different implant sites after 2 weeks in vivo relative to endogenous BAT (FVB/NJ; n = 5). I: Serum cytokine levels measured 2 weeks postimplantation of BAT-MACT or the same ADMSCs delivered via PBS. Animals were administered the 60% fat diet for the duration of this study (C57BL/6J; n = 6). IL, interleukin. Significance at **P < 0.01 and ***P < 0.001. More
Images
Regions with variations in histone H3K9Ac levels in monocytes of the case a...
Published: 12 April 2014
Figure 4 Regions with variations in histone H3K9Ac levels in monocytes of the case and control groups, and the biological functions related to the annotated promoters in these regions. A: Hierarchical clustering of hyperacetylated regions in case and control groups. The H3K9 hyperacetylated regions (age- and gender-adjusted nominal P < 0.05, fold change ≥1.1) in the case and control groups were pooled, and the acetylation levels were calculated for each region by averaging the log2 ratios of probes falling into these regions. The acetylation levels were mean centered across the 60 samples, and hierarchical clustering of these regions was generated using the average linkage method with Pearson correlation as the similarity metric and visualized by Java TreeView version 2.1. Blue represents acetylation levels above the mean, and yellow represents acetylation levels below the mean. The annotated genes containing a hyperacetylated region in their promoters are shown on the right. For regions located in the promoters of more than one gene, all the corresponding gene symbols are listed (separated by commas). For multiple regions located within the same gene promoter, the same gene symbol is listed for each region. Thus, 39 case hyperacetylated regions (spanning the promoters of 38 genes) and 8 control hyperacetylated regions (spanning the promoters of 8 genes) are depicted. B: IPA of H3K9 hyperacetylated promoters in case subjects (in silico analyses). The 38 genes identified in case subject samples that have H3K9 hyperacetylated regions in their promoters (−3,200 to 800 bp of TSS) were imported into IPA for identification of overrepresented canonical pathways. The 162 pathways in IPA knowledge-based database were sorted by P values (Fisher’s exact test P values adjusted by the Bonferroni-Holm [B-H] method), and the top 10 pathways are shown. Blue bars represent −log10 (P value) of pathways. The B-H–adjusted P values of the enrichments of all the 10 pathways are <0.0025. IL, interleukin; IRF, interferon regulator factor; PKR, RNA-dependent protein kinase; Hyper, hyperacetylation. Figure 4. Regions with variations in histone H3K9Ac levels in monocytes of the case and control groups, and the biological functions related to the annotated promoters in these regions. A: Hierarchical clustering of hyperacetylated regions in case and control groups. The H3K9 hyperacetylated regions (age- and gender-adjusted nominal P < 0.05, fold change ≥1.1) in the case and control groups were pooled, and the acetylation levels were calculated for each region by averaging the log2 ratios of probes falling into these regions. The acetylation levels were mean centered across the 60 samples, and hierarchical clustering of these regions was generated using the average linkage method with Pearson correlation as the similarity metric and visualized by Java TreeView version 2.1. Blue represents acetylation levels above the mean, and yellow represents acetylation levels below the mean. The annotated genes containing a hyperacetylated region in their promoters are shown on the right. For regions located in the promoters of more than one gene, all the corresponding gene symbols are listed (separated by commas). For multiple regions located within the same gene promoter, the same gene symbol is listed for each region. Thus, 39 case hyperacetylated regions (spanning the promoters of 38 genes) and 8 control hyperacetylated regions (spanning the promoters of 8 genes) are depicted. B: IPA of H3K9 hyperacetylated promoters in case subjects (in silico analyses). The 38 genes identified in case subject samples that have H3K9 hyperacetylated regions in their promoters (−3,200 to 800 bp of TSS) were imported into IPA for identification of overrepresented canonical pathways. The 162 pathways in IPA knowledge-based database were sorted by P values (Fisher’s exact test P values adjusted by the Bonferroni-Holm [B-H] method), and the top 10 pathways are shown. Blue bars represent −log10 (P value) of pathways. The B-H–adjusted P values of the enrichments of all the 10 pathways are <0.0025. IL, interleukin; IRF, interferon regulator factor; PKR, RNA-dependent protein kinase; Hyper, hyperacetylation. More
Images
Serum concentrations (in NPX units) of the three biomarkers of inflammation...
Published: 19 February 2021
Figure 3 Serum concentrations (in NPX units) of the three biomarkers of inflammation which showed at least one pairwise difference between subgroups after adjustment for clustering variables. Data are shown as median ± 25th/75th percentiles. CASP8, caspase-8; EN-RAGE, S100 calcium-binding protein ... More
Journal Articles
Journal: Diabetes
Diabetes 1995;44(10):1233–1238
Published: 01 October 1995
... unclear, recent studies associate interleukin (IL) 6 with mesangial proliferative glomerulonephritis. To elucidate the expression and localization of IL-6 mRNA in renal tissues of patients with DN, a high-resolution in situ hybridization using digoxigenin-labeled oligonucleotide was performed. Patients...
Journal Articles
Journal: Diabetes
Diabetes 2002;51(11):3347–3349
Published: 01 November 2002
... that interleukin (IL)-18 acts as a proinflammatory cytokine and, in synergy with IL-12, promotes development of Th1 lymphocyte response by induction of γ-interferon production. The aim of our study was to evaluate the frequency of known polymorphisms in the IL-18 promoter in patients with type 1 diabetes...
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Schematic view of the proposed role of plasma ceramide in the development o...
Published: 17 January 2013
FIG. 1. Schematic view of the proposed role of plasma ceramide in the development of skeletal muscle insulin resistance. In this model, ceramides are packaged with LDL in the liver and released into the circulation where they target skeletal muscle in two specific ways. First, LDL-ceramide is inte... More