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Articles by A Ruokonen
Total Records ( 3 ) for A Ruokonen
  R. M Freathy , A. J Bennett , S. M Ring , B Shields , C. J Groves , N. J Timpson , M. N Weedon , E Zeggini , C. M Lindgren , H Lango , J. R.B Perry , A Pouta , A Ruokonen , E Hypponen , C Power , P Elliott , D. P Strachan , M. R Jarvelin , G. D Smith , M. I McCarthy , T. M Frayling and A. T. Hattersley
  OBJECTIVE

Low birth weight is associated with an increased risk of type 2 diabetes. The mechanisms underlying this association are unknown and may represent intrauterine programming or two phenotypes of one genotype. The fetal insulin hypothesis proposes that common genetic variants that reduce insulin secretion or action may predispose to type 2 diabetes and also reduce birth weight, since insulin is a key fetal growth factor. We tested whether common genetic variants that predispose to type 2 diabetes also reduce birth weight.

RESEARCH DESIGN AND METHODS

We genotyped single-nucleotide polymorphisms (SNPs) at five recently identified type 2 diabetes loci (CDKAL1, CDKN2A/B, HHEX-IDE, IGF2BP2, and SLC30A8) in 7,986 mothers and 19,200 offspring from four studies of white Europeans. We tested the association between maternal or fetal genotype at each locus and birth weight of the offspring.

RESULTS

We found that type 2 diabetes risk alleles at the CDKAL1 and HHEX-IDE loci were associated with reduced birth weight when inherited by the fetus (21 g [95% CI 11–31], P = 2 x 10–5, and 14 g [4–23], P = 0.004, lower birth weight per risk allele, respectively). The 4% of offspring carrying four risk alleles at these two loci were 80 g (95% CI 39–120) lighter at birth than the 8% carrying none (Ptrend = 5 x 10–7). There were no associations between birth weight and fetal genotypes at the three other loci or maternal genotypes at any locus.

CONCLUSIONS

Our results are in keeping with the fetal insulin hypothesis and provide robust evidence that common disease-associated variants can alter size at birth directly through the fetal genotype.

  D Canoy , A Pouta , A Ruokonen , A. L Hartikainen , P Saikku and M. R. Jarvelin
 

Context: Impaired fetal growth is associated with increased risk for coronary heart disease and diabetes in adulthood, but the underlying mechanism is unclear.

Objective: The objective of the study was to examine the relation between early growth (weight at birth and first year) and adult total leukocyte count, the primary cell effectors of inflammation.

Design: This was a birth cohort study (Northern Finland Birth Cohort 1966) with participants prospectively and longitudinally followed up from birth to age 31 yr.

Setting: This was a general population-based cohort in Finland.

Participants: A total of 5619 offspring of expectant mothers who attended a clinical examination and blood draw at 31-yr follow-up (4486 with complete data on weight at 1 yr) participated in the study.

Main Exposure Variables: Weight at birth and at 1 year.

Main Outcome Measure: Absolute leukocyte count was measured.

Results: Total leukocyte count was lower at higher birth weight categories with or without adjustments for adult systolic blood pressure, total cholesterol, fasting insulin, body mass index, cigarette smoking, sex, gestational age, and other life course factors. The covariate-adjusted regression coefficient for log-transformed total leukocyte count (x 109 cells/liter) per 1 sd (525 g) increase in birth weight was –0.012 (95% confidence interval –0.021 to –0.004). The association persisted, even when limiting our analyses among healthy and nonsmoking individuals, and the inversely linear relation was steepest among those with lower weight attained at 1 yr (P for interaction = 0.027).

Conclusion: Poorer growth in early life was associated with systemic low-grade inflammation in adulthood. This relation suggests a plausible inflammatory mechanism linking early growth impairment with risk of coronary heart disease and diabetes later in life.

  J Puurunen , T Piltonen , P Jaakkola , A Ruokonen , L Morin Papunen and J. S. Tapanainen
 

Introduction: Hyperandrogenism is one of the main features of polycystic ovary syndrome (PCOS). Of circulating androgens, 50% of androstenedione and testosterone are of ovarian and adrenal origin, whereas dehydroepiandrosterone (DHEA) and DHEA sulfate are almost uniquely of adrenal origin. Our previous studies have indicated that ovarian androgen production capacity is enhanced in women with PCOS, and it remains high until late reproductive age. To study whether this also applies to adrenal androgen production, ACTH tests were performed in healthy women and in women with PCOS.

Materials: Sixty-nine healthy women (aged 19–62 yr; body mass index 19.2–35.0 kg/m2) and 58 women with previously diagnosed PCOS (aged 18–59 yr; body mass index 19.0–42.9 kg/m2) participated in the study.

Methods: The subjects underwent ACTH stimulation tests, and serum cortisol, 17-hydroxyprogesterone, androstenedione, testosterone, DHEA, and DHEA sulfate levels were analyzed at 0, 30, and 60 min.

Results: Basal and ACTH-stimulated levels of most adrenal androgens decreased in healthy women with age, whereas in women with PCOS, only the concentrations of basal serum 17-hydroxyprogesterone decreased, and all areas under the curve (AUCs) remained unchanged and significantly higher (except for DHEA) than those in control women. Likewise, at the menopausal transition, pre- and postmenopausal women with PCOS exhibited mainly unchanged and higher basal androgen and AUC levels.

Conclusions: Similarly to ovarian endocrine function, serum adrenal steroid levels and adrenal steroid production capacity remain enhanced at least up to menopause in women with PCOS.

 
 
 
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