[Clinicogenetic aspects of carbohydrate metabolism disorders and efficacy of their correction with moxonidine and metformine in patients with arterial hypertension].
OBJECTIVE
To study effects of monotherapy with moxonidine and metformine on metabolic parameters in hypertensive patients with carbohydrate dysbolism (CD) regarding polymorphic markers of genes PPARalpha, PPARgamma and IRS type 1 and 2.


METHODS
A total of 83 patients (31 male and 52 female patients aged 40-75 years) with untreated arterial hypertension stage I, obesity and CD (by glucose tolerance test) entered the trial. The patients were randomized into two groups. Patients of group I (n=42) received moxonidin in a dose 0.4 mg/day, of group 2 (n=41)--metformin in a dose 1000 mg/day. Measurement of arterial pressure, blood count and biochemistry, oral test for glucose tolerance with glucose and insulin measurement before meal and 1, 2 and 3 hours later was made initially and on the treatment week 16 Genotypes of polymorphic markers of genes PPARA, PPARG2, IRS1 and IRS2 were defined in all the patients.


RESULTS
Changes in basic hemodynamic and metabolic indices in therapy with moxonidine depending on polymorphic markers of genes PPARA, PPARG2, IRS1 and IRS2 in patients with AH and CD showed that G allele PPARG2 is associated with greater weight loss, G allele PPARA--with weight loss, C allele PPARA--with maximal fall of diastolic blood pressure.


CONCLUSIONS
Genetic factors participate in development of metabolic disturbances in hypertensive patients, obesity and CD and determine treatment efficacy in each individual patient.
Kobalava
Zh D
ZhD
Tolkacheva
V V
VV
Ignat'ev
I V
IV
Glezer
M G
MG
Kuzin
A I
AI
Karpov
Iu A
IuA
Konradi
A O
AO
Zheleznykh
E A
EA
D000328:Adult; D000368:Aged; D000483:Alleles; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D050260:Carbohydrate Metabolism; D004247:DNA / Q000187:drug effects / Q000235:genetics; D005260:Female; D005500:Follow-Up Studies; D005819:Genetic Markers / Q000187:drug effects / Q000235:genetics; D044882:Glucose Metabolism Disorders / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000235:genetics*; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications / Q000235:genetics*; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007093:Imidazoles / Q000627:therapeutic use*; D007328:Insulin / Q000097:blood; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; D008297:Male; D008687:Metformin / Q000627:therapeutic use*; D008875:Middle Aged; D047493:PPAR alpha / Q000097:blood / Q000187:drug effects / Q000235:genetics; D047495:PPAR gamma / Q000097:blood / Q000187:drug effects / Q000235:genetics; D010750:Phosphoproteins / Q000097:blood / Q000187:drug effects / Q000235:genetics; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000187:drug effects / Q000235:genetics*; D016896:Treatment Outcome
D000959:Antihypertensive Agents; D005819:Genetic Markers; D007004:Hypoglycemic Agents; C526292:IRS1 protein, human; C526297:IRS2 protein, human; D007093:Imidazoles; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; D047493:PPAR alpha; D047495:PPAR gamma; D010750:Phosphoproteins; D004247:DNA; D008687:Metformin; C043482:moxonidine