Abstract

Recent basic studies indicate that adiponectin, a key factor in the metabolic syndrome (MetS), directly regulates calcium (Ca)-phosphorus (P) metabolism. Previous studies indicate that serum P levels are inversely associated with the MetS in the general population. In this study, we investigated the association of serum P levels with the MetS and plasma adiponectin levels in both type 2 diabetes patients (T2D) and nondiabetic individuals (non-DM). We included 487 subjects with normal kidney function (eGFR ≥ 60 mL/min/1.73m2), including 285 T2D and 202 non-DM. The MetS was diagnosed according to the criteria of AHA/NHLBI. The medians of plasma adiponectin level and serum P level in the total population were 6.6 µg/mL, 3.6 mg/dL, respectively. T2D had older age, greater BMI, higher P levels, lower adiponectin levels, and comparable serum Ca levels and eGFR compared to non-DM. The MetS was diagnosed in 31% of non-DM and in 77% of T2D. In non-DM, but not in T2D, serum P levels tended to be lower in subjects with MetS than those without MetS, and were significantly lower in those having multiple MetS components. Plasma adiponectin levels were lower in subjects with MetS than those without MetS in both groups. Serum P levels showed inverse correlation with a number of MetS-related parameters, among which adiponectin level was the strongest one (ρ=0.338, p<0.001), in non-DM, but not in T2D. Multivariate analysis revealed that serum P levels were positively associated with plasma adiponectin levels (β=0.257, p=0.009), independently of age, BMI, eGFR, and serum Ca levels in non-DM women. On the other hand, no association was found between serum P and adiponectin levels in T2D. These data indicate that serum P levels, which are lower in the MetS, are independently and positively associated with plasma adiponectin levels in non-DM women. This study suggests a direct relationship between adiponectin and serum P level in women, which may be dysregulated in T2D. Disclosure Y. Natsuki: None. T. Morioka: Research Support; Self; Eli Lilly and Company, Merck & Co., Inc., Mitsubishi Tanabe Pharma Corporation, Novartis Pharmaceuticals Corporation, Sanofi K.K., Takeda Pharmaceutical Company Limited. Speaker's Bureau; Self; Astellas Pharma Inc., AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Merck & Co., Inc., Novo Nordisk Inc., Roche Diagnostics K.K., Sanofi K.K., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Other Relationship; Self; Ono Pharmaceutical Co., Ltd. Y. Kakutani: None. Y. Yamazaki: None. M. Kurajoh: None. K. Mori: Speaker's Bureau; Self; Boehringer Ingelheim International GmbH, Eli Lilly and Company, Mitsubishi Tanabe Pharma Corporation, Ono Pharmaceutical Co., Ltd. S. Fukumoto: Research Support; Self; Astellas Pharma Inc., Chugai Pharmaceutical Co., Ltd., Kowa Pharmaceutical Europe Co. Ltd., Mitsubishi Tanabe Pharma Corporation, Taisho Toyama Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Speaker's Bureau; Self; Novo Nordisk Inc., Sanofi K.K. A. Shioi: None. T. Shoji: Research Support; Self; Bayer Yakuhin, Ltd., Chugai Pharmaceutical Co., Ltd., Ono Pharmaceutical Co., Ltd. Speaker's Bureau; Self; Kissei Pharmaceutical Co., Ltd., Kowa, Kyowa Hakko Kirin Co., Ltd. Y. Imanishi: Speaker's Bureau; Self; Chugai Clinical Research Center Co., Ltd., Daiichi Sankyo Company, Limited, Kyowa Hakko Kirin Co., Ltd., Ono Pharmaceutical Co., Ltd. M. Emoto: Research Support; Self; Ono Pharmaceutical Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd. Speaker's Bureau; Self; Astellas Pharma Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Kowa Pharmaceutical Co., Ltd., Kyowa Hakko Kirin Co., Ltd., Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi, Sumitomo Dainippon Pharma Co., Ltd., Taisho Toyama Pharmaceutical CO., Ltd., Takeda Pharmaceutical Company Limited. M. Inaba: None.

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