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Johan Styrud and Ulf J. Eriksson


In order to elucidate cellular mechanisms causing skeletal malformations in offspring of diabetic rats we studied the incorporation of thymidine and sulphate into embryonic (pre)chondrocytes exposed to increased levels of D-glucose and β-hydroxybutyric acid for six days in vitro. The (pre)chondrocytes were prepared from embryos of normal or diabetic rats of a malformation-prone strain or from embryos of normal rats of a non-malformation-prone strain. Diabetic female rats of the former strain are known to produce a high proportion of offspring with mandibular and lumbosacral malformations. Increased β-hydroxybutyric acid caused decreased thymidine incorporation in all types of chondrocytes, and decreased sulphate incorporation in limb bud cells from embryos of normal rats from both strains. Elevated D-glucose levels yielded a slight decrease in thymidine incorporation in mandibular arch cells from embryos of normal rats of the malformation-prone strain, and a marked decrease of both sulphate and thymidine incorporation in mandibular arch cells from embryos of diabetic rats of this strain. The observations suggest that elevated levels of D-glucose or β-hydroxybutyric acid are able to inhibit the differentiation and growth of (pre)chondrocytes and illustrate a selective sensitivity of mandibular arch (pre)chondrocytes to a diabetic environment. The data are compatible with the view that both D-glucose and β-hydroxybutyric acid may cause aberrations in the development of rat mandibular arch chondrocytes, suggesting a role for these compounds in diabetic teratogenesis.

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Anja I Franssila-Kallunki, Johan G Eriksson, and Leif C Groop

The present study was undertaken to compare the effect of hyperglycemia and euglycemia during identical hyperinsulinemic conditions on glucose metabolism in NIDDM subjects. Eight NIDDM subjects participated in a 4 h hyperglycemic (12.1±0.7 mmol/l), hyperinsulinemic (475±43 pmol/l) and in a 4 h euglycemic (5.5±0.5 mmol/l), hyperinsulinemic (468±36 pmol/l) insulin clamp in combination with indirect calorimetry and [3H]-3-glucose. Six non-diabetic subjects were studied during euglycemia (5.1±0.2 mmol/l) and hyperinsulinemia (474±35 pmol/l) and served as controls. In NIDDM patients the rate of insulin-stimulated glucose disposal was 57% greater during hyperglycemia compared with euglycemia throughout the 4 h clamp (p<0.01). The major part of the increase in glucose metabolism during hyperglycemia was due to an increase in the non-oxidative glucose metabolism (89%). Whereas glucose metabolism could not be normalized during the prolonged euglycemic hyperinsulinemic clamp in NIDDM patients (49.9±6.8 vs 57.5±5.4 μmol·(kgLBM)−1·min−1 in controls) the addition of hyperglycemia resulted in complete normalization of the glucose disposal rates (78.3±5.8 μmol·(kgLBM)−1·min−1). The effect of hyperglycemia was apparent already at 60 min of the clamp. The data thus suggest that glucose metabolism in NIDDM is insulin resistant, but that the defect in insulin-stimulated glucose uptake can be overcome by increasing the glucose concentration.

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Elisabeth IM Widén, Johan G Eriksson, Agneta V Ekstrand, and Leif C Groop

A possible pathogenetic link between absence of first-phase insulin secretion and development of impaired glucose metabolism has been suggested by the results of several cross-sectional studies. First-phase insulin secretion measured during a + 7 mmol/l hyperglycemic glucose clamp correlated with total glucose disposal during the clamp (r = 0.65, p <0.001, N = 59). To examine whether restoration of first-phase insulin secretion improves peripheral glucose uptake in subjects with impaired glucose utilization, seven insulin-resistant subjects (age 54 (38–62) years; BMI 29.3 (21.7–35.8); fasting plasma glucose 5.5 (4.8–7.2) mmol/l; fasting insulin 57 (37–105) pmol/l with impaired first-phase (148 (29–587) vs controls 485 (326–1086) pmol/l× 10 min; p<0.05) and normal second-phase (1604 (777–4480) vs controls (1799 (763–2771) pmol/l × 110 min) insulin secretion were restudied. The impaired first-phase insulin secretion was restored by an iv insulin bolus at the start of the hyperglycemic clamp. Substrate oxidation rates and hepatic glucose production were determined by indirect calorimetry and [3-3H]glucose infusion. Total glucose uptake was impaired in the insulinresistant subjects with impaired first-phase insulin secretion compared to controls (18.8 (13.2–22.2) vs 34.8 (24.3–62.1) μmol·kg−1·min−1; p<0.01). Restoration of first-phase insulin secretion (1467 (746–2440) pmol/l× 10 min) did not affect glucose uptake (20.2 (9.9–23.8) μmol·kg−1·min−1), with no difference in oxidative and non-oxidative glucose metabolism between the experiments. Second-phase insulin secretion was similar during both experiments. We conclude that although first-phase insulin secretion correlates with total glucose uptake, replacement of impaired first-phase insulin secretion does not improve glucose uptake in subjects with impaired glucose disposal and normal second-phase insulin secretion. The data dispute a causal relationship between first-phase insulin secretion and impaired glucose uptake in these subjects.

Open access

Marika Paalanne, Marja Vääräsmäki, Sanna Mustaniemi, Marjaana Tikanmäki, Karoliina Wehkalampi, Hanna-Maria Matinolli, Johan Eriksson, Marjo-Riitta Jarvelin, Laure Morin-Papunen, and Eero Kajantie


It has been suggested that adverse early life exposures increase the risk of developing polycystic ovary syndrome (PCOS) in later life. We hypothesized that women born preterm would have more biochemical and clinical signs of PCOS than women born at term.


The ESTER Preterm Birth Study participants were born in Northern Finland, and identified from the Northern Finland Birth Cohort and the Finnish Medical Birth Register. Altogether, 74 women born very or moderately preterm (<34 gestational weeks, VMPT), 127 born late preterm (at 34–36 weeks, LPT), and 184 born full term (≥37 weeks, controls) were included in the analysis (mean age 23.2y).


We measured serum total testosterone and sex hormone binding globulin (SHBG) and calculated free androgen index (FAI). PCOS according to the clinical and biochemical signs was defined either as hirsutism and oligoamenorrhea (via questionnaire), or as oligoamenorrhea and elevated testosterone levels (>2.4 nmol/l).


Women born VMPT/LPT exhibited 33.0% (8.7, 62.8)/16.4% (-2.0, 38.1) higher testosterone, 28.5% (5.3, 45.9)/24.1% (5.6, 38.9) lower SHBG levels, and 64.6% (19.4, 127.1)/ 42.5% (11.1, 82.9) higher FAI than controls after adjusting for age and recruitment cohort, maternal BMI, smoking, and pregnancy disorders, parental education, history of hypertension, diabetes, myocardial infarction or stroke, and subject’s birth weight SD. Odds ratios for having PCOS were 1.67 (0.44, 6.23)/3.11 (1.26, 7.70).


Women born preterm have a more hyperandrogenic hormonal profile, and those born LPT are approximately three times more likely at risk to have PCOS compared to women born at term.

Free access

Ville Huovinen, Kaisa K Ivaska, Riku Kiviranta, Marco Bucci, Heta Lipponen, Samuel Sandboge, Juho Raiko, Johan G Eriksson, Riitta Parkkola, Patricia Iozzo, and Pirjo Nuutila


Non-pharmacological interventions are important in reducing risk for osteoporotic fractures. We investigated the effects of a 16-week individualized resistance training intervention on bone mineral density (BMD), bone turnover markers and 10-year relative risk (RR) for osteoporotic fracture.


Interventional study with a follow-up.


In total, 37 elderly women (mean age 71.9 ± 3.1 years) with decreased muscle strength participated in the resistance training intervention three times per week with 60 min per session for 16 weeks under the supervision of a licensed physiotherapist. Total hip BMD with quantitative CT, bone markers (sclerostin, osteocalcin, CTX, PINP, IGF-1, 25(OH)-D) and 10-year RR for osteoporotic fracture were measured at baseline, post-intervention and at 1-year follow-up after the end of the intervention. Eleven age- and sex-matched controls did not participate in the intervention but were studied at baseline and at 1-year follow-up.


Resistance training seemed to increase total hip BMD by 6% (P = 0.005). Sclerostin (P < 0.001) and total osteocalcin (P = 0.04) increased while other bone markers remained unchanged. A 10-year RR for major osteoporotic and hip fracture remained unchanged. At follow-up total hip BMD (P < 0.001) decreased back to the baseline level with a simultaneous decrease in serum sclerostin (P = 0.045), CTX (P < 0.001) and an increase in 25(OH)-D (P < 0.001), 10-year RR for major osteoporotic (P = 0.002) and hip fracture (P = 0.01).


Our findings suggest an important role of continuous supervised resistance training for the prevention of osteoporotic fractures in elderly women with decreased muscle strength.