Genetic polymorphisms of the renin-angiotensin system and obesity-related metabolic changes in response to low-energy diets in obese women.
OBJECTIVE
Genetic polymorphisms of the renin-angiotensin system have been implicated in cardiovascular and metabolic diseases. The purpose of this study was to investigate whether the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene and 3123C/A polymorphism of the angiotensin II type 2 receptor (AT(2)R) gene affect blood pressure and other obesity-related metabolic changes in response to low-energy diets using meal replacement shakes for weight loss.


METHODS
Clinical, metabolic, and biochemical profiles were measured before and after a 2-mo intervention in 32 obese women (age 49.9 ± 8.4 [SD] y; BMI 28.4 ± 3.3 kg/m²) restricted to 1200 kcal/d (5021 kJ/d). The polymorphisms were determined with an intercalater-mediated FRET probe assay system.


RESULTS
Although weight loss and nutrient intake levels did not differ among the genotypes, the reduction in body fat after weight loss was significantly less in the ACE deletion/deletion (D/D) genotype than insertion/insertion (I/I) plus I/D genotype (-2.25 ± 1.40% versus -0.80 ± 1.57%, P < 0.05). The AT₂R A/A group had significantly less improved levels of systolic blood pressure (-7.23 ± 8.50 versus 2.50 ± 12.6 mmHg, P < 0.05), low-density lipoprotein-cholesterol (-0.36 ± 0.29 versus -0.09 ± 0.25 mmol/L, P < 0.05), carbohydrate (-54.4 ± 27.2 versus -31.8 ± 16.3 mg/min, P < 0.05) and fat oxidation (8.31 ± 11.86 versus 0.05 ± 9.99 mg/min, P < 0.05) than the C/C plus C/A genotypes.


CONCLUSIONS
The present findings suggest that the homozygous form of the ACE gene may hinder the improvement of body fat and that the homozygous form of the AT₂R gene may make improving systolic blood pressure and some obesity-related metabolic parameters through a dietary intervention difficult among obese women.
Hamada
Taku
T
Graduate School of Sport and Exercise Science, Osaka University of Health and Sport Sciences, Osaka, Japan. Electronic address: hamada@ouhs.ac.jp.
Kotani
Kazuhiko
K
Department of Clinical Laboratory Medicine, Jichi Medical University, Tochigi, Japan.
Nagai
Narumi
N
School of Human Science and Environment, University of Hyogo, Hyogo, Japan.
Tsuzaki
Kokoro
K
Division of Preventive Medicine, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto, Japan.
Sano
Yoshiko
Y
Division of Preventive Medicine, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto, Japan.
Matsuoka
Yukiyo
Y
Division of Preventive Medicine, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto, Japan.
Fujibayashi
Mami
M
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Kiyohara
Natsuki
N
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Tanaka
Seitaro
S
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Yoshimura
Makiko
M
Institute for Health Care Science, SUNTORY WELLNESS Ltd., Osaka, Japan.
Egawa
Kahori
K
Institute for Health Care Science, SUNTORY WELLNESS Ltd., Osaka, Japan.
Kitagawa
Yoshinori
Y
Institute for Health Care Science, SUNTORY WELLNESS Ltd., Osaka, Japan.
Kiso
Yoshinobu
Y
Institute for Health Care Science, SUNTORY WELLNESS Ltd., Osaka, Japan.
Moritani
Toshio
T
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Sakane
Naoki
N
Division of Preventive Medicine, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto, Japan.
D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D001794:Blood Pressure / Q000235:genetics*; D031204:Caloric Restriction; D050260:Carbohydrate Metabolism / Q000235:genetics; D008078:Cholesterol, LDL / Q000097:blood / Q000235:genetics; D004038:Diet, Reducing; D005260:Female; D005838:Genotype; D006801:Humans; D015227:Lipid Peroxidation / Q000235:genetics; D008875:Middle Aged; D009765:Obesity / Q000178:diet therapy / Q000235:genetics* / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics*; D012084:Renin-Angiotensin System / Q000235:genetics
D008078:Cholesterol, LDL; D044139:Receptor, Angiotensin, Type 2; D007703:Peptidyl-Dipeptidase A