Relationships between serum soluble leptin receptor level and serum leptin and adiponectin levels, insulin resistance index, lipid profile, and leptin receptor gene polymorphisms in the Japanese population.
Leptin plays an important role in the regulation of body weight and is known to circulate in both free and bound forms. One of the leptin receptor isoforms exists in a circulating soluble form that can bind leptin. Clinical studies have shown that soluble leptin receptor (sOB-R) levels are lower in obese individuals. In the present study, we measured the serum sOB-R level in 419 healthy Japanese subjects (198 men and 221 women, aged 30 to 65 years, body mass index [BMI] 21.7 +/- 2.6 [SD] kg/m2) and in 150 type 2 diabetic patients (96 men and 54 women, BMI 24.3 +/- 3.8 kg/m2). We investigated the relationships between serum sOB-R level and BMI, blood pressure, homeostasis model assessment-insulin resistance index (HOMA-IR), serum leptin and adiponectin levels, lipid profile, and leptin receptor (LEPR) gene Lys109Arg and Gln223Arg polymorphisms. Serum leptin and sOB-R levels were measured by radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA), respectively. The serum sOB-R level in men was significantly higher than that in women. The serum sOB-R level was negatively correlated with BMI, fasting insulin, HOMA-IR, and serum leptin level and positively correlated with high-density lipoprotein (HDL)-cholesterol and serum adiponectin levels. The correlations between serum sOB-R level and fasting insulin, HOMA-IR, serum leptin, adiponectin, and HDL-cholesterol levels were significant even after adjustment for age, sex, and BMI in healthy subjects. There was no association between serum sOB-R level and the LEPR polymorphisms examined. These findings suggest that the serum sOB-R level is negatively correlated with HOMA-IR and serum leptin level and positively correlated with HDL-cholesterol level and serum adiponectin level, independent of age, sex, and BMI, in the Japanese population.
Ogawa
Takeo
T
Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Hirose
Hiroshi
H
Yamamoto
Yukihiro
Y
Nishikai
Kanako
K
Miyashita
Kiichi
K
Nakamura
Haruo
H
Saito
Ikuo
I
Saruta
Takao
T
D052242:Adiponectin; D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D015992:Body Mass Index; D015342:DNA Probes; D003924:Diabetes Mellitus, Type 2 / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D036341:Intercellular Signaling Peptides and Proteins; D007564:Japan; D020738:Leptin / Q000097:blood*; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D011153:Population; D011506:Proteins / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000097:blood* / Q000235:genetics*; D054411:Receptors, Leptin; D020133:Reverse Transcriptase Polymerase Chain Reaction
D052242:Adiponectin; D015342:DNA Probes; D036341:Intercellular Signaling Peptides and Proteins; C515448:LEPR protein, human; D020738:Leptin; D008055:Lipids; D011506:Proteins; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin