Bezafibrate, a peroxisome proliferator–activated receptor α agonist, decreases circulating CD14+CD16+ monocytes in patients with type 2 diabetes
CD14+CD16+ monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14+CD16+ monocytes is increased in patients with chronic renal failure or coronary artery disease. We investigated the effect of bezafibrate, a peroxisome proliferat...
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| Published in | Translational research : the journal of laboratory and clinical medicine Vol. 165; no. 2; pp. 336 - 345 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.02.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1931-5244 1878-1810 1878-1810 |
| DOI | 10.1016/j.trsl.2014.07.008 |
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| Abstract | CD14+CD16+ monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14+CD16+ monocytes is increased in patients with chronic renal failure or coronary artery disease. We investigated the effect of bezafibrate, a peroxisome proliferator–activated receptor α agonist, on circulating CD14+CD16+ monocytes in patients with type 2 diabetes. Using cells isolated from type 2 diabetic subjects, we also examined the in vitro expression of CD16 messenger RNA (mRNA) by mononuclear cells (MNCs) exposed to bezafibrate. The percentage of CD14+CD16+ monocytes among all CD14+ monocytes was significantly higher in subjects with impaired glucose tolerance (P < 0.01) or type 2 diabetes (P < 0.05) than in those with normal glucose tolerance. The percentage of CD14+CD16+ monocytes was significantly lower in patients with type 2 diabetes who were taking bezafibrate (400 mg/d) than in patients not taking it (P < 0.01). Treatment with bezafibrate for 12 weeks significantly reduced the percentage of circulating CD14+CD16+ monocytes from 45.4 ± 25.2% to 38.3 ± 21.8% (P = 0.0144). In an in vitro study, the expression of CD16 mRNA by MNCs from 6 diabetic subjects was decreased after 24 hours of treatment with 10 μg/mL of bezafibrate (P < 0.05). Expression of IL-1β mRNA by MNCs was also decreased after 24 hours of treatment with 10 μg/mL of bezafibrate, whereas the IL-1β level in the culture supernatant was significantly decreased after treatment of MNCs with either 1 or 10 μg/mL of bezafibrate. In conclusion, bezafibrate decreased circulating CD14+CD16+ monocytes in patients with type 2 diabetes, probably by inhibiting the expression of CD16 mRNA. |
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| AbstractList | CD14+ CD16+ monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14+ CD16+ monocytes is increased in patients with chronic renal failure or coronary artery disease. We investigated the effect of bezafibrate, a peroxisome proliferator–activated receptor α agonist, on circulating CD14+ CD16+ monocytes in patients with type 2 diabetes. Using cells isolated from type 2 diabetic subjects, we also examined the in vitro expression of CD16 messenger RNA (mRNA) by mononuclear cells (MNCs) exposed to bezafibrate. The percentage of CD14+ CD16+ monocytes among all CD14+ monocytes was significantly higher in subjects with impaired glucose tolerance ( P < 0.01) or type 2 diabetes ( P < 0.05) than in those with normal glucose tolerance. The percentage of CD14+ CD16+ monocytes was significantly lower in patients with type 2 diabetes who were taking bezafibrate (400 mg/d) than in patients not taking it ( P < 0.01). Treatment with bezafibrate for 12 weeks significantly reduced the percentage of circulating CD14+ CD16+ monocytes from 45.4 ± 25.2% to 38.3 ± 21.8% ( P = 0.0144). In an in vitro study, the expression of CD16 mRNA by MNCs from 6 diabetic subjects was decreased after 24 hours of treatment with 10 μg/mL of bezafibrate ( P < 0.05). Expression of IL-1β mRNA by MNCs was also decreased after 24 hours of treatment with 10 μg/mL of bezafibrate, whereas the IL-1β level in the culture supernatant was significantly decreased after treatment of MNCs with either 1 or 10 μg/mL of bezafibrate. In conclusion, bezafibrate decreased circulating CD14+ CD16+ monocytes in patients with type 2 diabetes, probably by inhibiting the expression of CD16 mRNA. CD14+CD16+ monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14+CD16+ monocytes is increased in patients with chronic renal failure or coronary artery disease. We investigated the effect of bezafibrate, a peroxisome proliferator–activated receptor α agonist, on circulating CD14+CD16+ monocytes in patients with type 2 diabetes. Using cells isolated from type 2 diabetic subjects, we also examined the in vitro expression of CD16 messenger RNA (mRNA) by mononuclear cells (MNCs) exposed to bezafibrate. The percentage of CD14+CD16+ monocytes among all CD14+ monocytes was significantly higher in subjects with impaired glucose tolerance (P < 0.01) or type 2 diabetes (P < 0.05) than in those with normal glucose tolerance. The percentage of CD14+CD16+ monocytes was significantly lower in patients with type 2 diabetes who were taking bezafibrate (400 mg/d) than in patients not taking it (P < 0.01). Treatment with bezafibrate for 12 weeks significantly reduced the percentage of circulating CD14+CD16+ monocytes from 45.4 ± 25.2% to 38.3 ± 21.8% (P = 0.0144). In an in vitro study, the expression of CD16 mRNA by MNCs from 6 diabetic subjects was decreased after 24 hours of treatment with 10 μg/mL of bezafibrate (P < 0.05). Expression of IL-1β mRNA by MNCs was also decreased after 24 hours of treatment with 10 μg/mL of bezafibrate, whereas the IL-1β level in the culture supernatant was significantly decreased after treatment of MNCs with either 1 or 10 μg/mL of bezafibrate. In conclusion, bezafibrate decreased circulating CD14+CD16+ monocytes in patients with type 2 diabetes, probably by inhibiting the expression of CD16 mRNA. CD14(+)CD16(+) monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14(+)CD16(+) monocytes is increased in patients with chronic renal failure or coronary artery disease. We investigated the effect of bezafibrate, a peroxisome proliferator-activated receptor α agonist, on circulating CD14(+)CD16(+) monocytes in patients with type 2 diabetes. Using cells isolated from type 2 diabetic subjects, we also examined the in vitro expression of CD16 messenger RNA (mRNA) by mononuclear cells (MNCs) exposed to bezafibrate. The percentage of CD14(+)CD16(+) monocytes among all CD14(+) monocytes was significantly higher in subjects with impaired glucose tolerance (P < 0.01) or type 2 diabetes (P < 0.05) than in those with normal glucose tolerance. The percentage of CD14(+)CD16(+) monocytes was significantly lower in patients with type 2 diabetes who were taking bezafibrate (400 mg/d) than in patients not taking it (P < 0.01). Treatment with bezafibrate for 12 weeks significantly reduced the percentage of circulating CD14(+)CD16(+) monocytes from 45.4 ± 25.2% to 38.3 ± 21.8% (P = 0.0144). In an in vitro study, the expression of CD16 mRNA by MNCs from 6 diabetic subjects was decreased after 24 hours of treatment with 10 μg/mL of bezafibrate (P < 0.05). Expression of IL-1β mRNA by MNCs was also decreased after 24 hours of treatment with 10 μg/mL of bezafibrate, whereas the IL-1β level in the culture supernatant was significantly decreased after treatment of MNCs with either 1 or 10 μg/mL of bezafibrate. In conclusion, bezafibrate decreased circulating CD14(+)CD16(+) monocytes in patients with type 2 diabetes, probably by inhibiting the expression of CD16 mRNA.CD14(+)CD16(+) monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14(+)CD16(+) monocytes is increased in patients with chronic renal failure or coronary artery disease. We investigated the effect of bezafibrate, a peroxisome proliferator-activated receptor α agonist, on circulating CD14(+)CD16(+) monocytes in patients with type 2 diabetes. Using cells isolated from type 2 diabetic subjects, we also examined the in vitro expression of CD16 messenger RNA (mRNA) by mononuclear cells (MNCs) exposed to bezafibrate. The percentage of CD14(+)CD16(+) monocytes among all CD14(+) monocytes was significantly higher in subjects with impaired glucose tolerance (P < 0.01) or type 2 diabetes (P < 0.05) than in those with normal glucose tolerance. The percentage of CD14(+)CD16(+) monocytes was significantly lower in patients with type 2 diabetes who were taking bezafibrate (400 mg/d) than in patients not taking it (P < 0.01). Treatment with bezafibrate for 12 weeks significantly reduced the percentage of circulating CD14(+)CD16(+) monocytes from 45.4 ± 25.2% to 38.3 ± 21.8% (P = 0.0144). In an in vitro study, the expression of CD16 mRNA by MNCs from 6 diabetic subjects was decreased after 24 hours of treatment with 10 μg/mL of bezafibrate (P < 0.05). Expression of IL-1β mRNA by MNCs was also decreased after 24 hours of treatment with 10 μg/mL of bezafibrate, whereas the IL-1β level in the culture supernatant was significantly decreased after treatment of MNCs with either 1 or 10 μg/mL of bezafibrate. In conclusion, bezafibrate decreased circulating CD14(+)CD16(+) monocytes in patients with type 2 diabetes, probably by inhibiting the expression of CD16 mRNA. |
| Author | Terasawa, Tomoko Aso, Yoshimasa Fukushima, Maiko Omori, Kyoko Inukai, Toshihiko Momobayashi, Atsushi |
| Author_xml | – sequence: 1 givenname: Tomoko surname: Terasawa fullname: Terasawa, Tomoko organization: Department of Internal Medicine, Koshigaya Hospital, Dokkyo Medical University, Koshigaya, Saitama, Japan – sequence: 2 givenname: Yoshimasa surname: Aso fullname: Aso, Yoshimasa email: yaso@dokkyomed.ac.jp organization: Department of Endocrinology and Metabolism, Dokkyo Medical University, Mibu, Tochigi, Japan – sequence: 3 givenname: Kyoko surname: Omori fullname: Omori, Kyoko organization: Department of Molecular Genetic Testing, Joint Research Center, Koshigaya Hospital, Dokkyo Medical University, Koshigaya, Saitama, Japan – sequence: 4 givenname: Maiko surname: Fukushima fullname: Fukushima, Maiko organization: Mitsubishi Chemical Medience Corporation, Itabashi, Tokyo, Japan – sequence: 5 givenname: Atsushi surname: Momobayashi fullname: Momobayashi, Atsushi organization: Mitsubishi Chemical Medience Corporation, Itabashi, Tokyo, Japan – sequence: 6 givenname: Toshihiko surname: Inukai fullname: Inukai, Toshihiko organization: Department of Internal Medicine, Koshigaya Hospital, Dokkyo Medical University, Koshigaya, Saitama, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25134759$$D View this record in MEDLINE/PubMed |
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| Keywords | NGT IL PPAR MNCs TNF IGT mononuclear cells normal glucose tolerance tumor necrosis factor impaired glucose tolerance peroxisome proliferator-activated receptor interleukin |
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| Snippet | CD14+CD16+ monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14+CD16+ monocytes is... CD14+ CD16+ monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14+ CD16+ monocytes is... CD14(+)CD16(+) monocytes are proinflammatory cells that produce tumor necrosis factor and interleukin (IL)-1β. The number of circulating CD14(+)CD16(+)... |
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| SubjectTerms | Adult Bezafibrate - therapeutic use Cross-Sectional Studies Cytokines - metabolism Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - immunology Female Gene Expression - drug effects Glucose Intolerance - blood Glucose Intolerance - drug therapy Glucose Intolerance - immunology GPI-Linked Proteins - genetics GPI-Linked Proteins - metabolism Humans Inflammation Mediators - metabolism Internal Medicine Lipopolysaccharide Receptors - metabolism Male Middle Aged Monocytes - classification Monocytes - drug effects Monocytes - immunology PPAR alpha - agonists Receptors, IgG - genetics Receptors, IgG - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Translational Medical Research |
| Title | Bezafibrate, a peroxisome proliferator–activated receptor α agonist, decreases circulating CD14+CD16+ monocytes in patients with type 2 diabetes |
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