No abstract

Human placental GH (hPGH) replaces pituitary GH during pregnancy. hPGH is correlated to serum IGF-I in normal pregnancies and in pregnancies complicated by fetoplacental disorders. In gestational diabetes and type 2 diabetes no correlation between hPGH and IGF-I has been found. The relationship between hPGH and IGF-I in type 1 diabetes mellitus has not been investigated thoroughly. Furthermore, hPGH may be involved in the development of insulin resistance during pregnancy. In this prospective, longitudinal study, 51 type 1 diabetic subjects were followed with repeated blood sampling during pregnancy (median, 14 blood samples/subject; range, 8-26). Maternal concentrations of serum hPGH, IGF-I, and IGF-II were measured and compared with insulin requirements and birth characteristics. hPGH was detected from as early as 6 wk gestation. In all subjects, a rise in serum hPGH was observed during pregnancy, and the rise between wk 16 and 25 was correlated to the rise between wk 26 and 35 (P < 0.001). From wk 26 onward, the increase in hPGH values was significantly correlated to the birth weight, expressed as a z-score (r(s) = 0.54; P < 0.001), as were the absolute hPGH values. Also, a positive influence of hPGH on placental weight was found. Serum IGF-I values decreased significantly from the first to the second trimester (P < or = 0.021). Serum hPGH correlated to serum IGF-I from wk 24- 35, and changes in IGF-I followed the increase in hPGH between wk 26-35 (r(s) = 0.53; P < 0.001), as did IGF-II (r(s) = 0.37; P = 0.008). Changes in IGF-I and IGF-II between wk 26-35 also correlated to the birth weight z-score (P < or = 0.020), but only hPGH remained significant in multiple regression analysis. Similar results were found in the subgroup delivering at term. Interestingly, the increase in hPGH was not correlated to the increase in insulin requirements, nor was any consistent relationship revealed during each gestational period. In conclusion, our study suggests a role for hPGH in the regulation of both IGFs and fetal growth in type 1 diabetes. In contrast, the increase in insulin requirements during pregnancy in type 1 diabetic subjects could not be related to hPGH levels.

In the direct comparison of home video consultations vs standard outpatient treatment in type 2 diabetes mellitus, telemedicine was a safe and available option with favourable outcomes after six months treatment.

To compare the metabolic effect of coingestion of saturated and monounsaturated fats with potato, 12 subjects with non-insulin-dependent diabetes mellitus (NIDDM) received 300 g mashed potato alone or in combination with 40 g olive oil, 80 g olive oil, 50 g butter, or 100 g butter, respectively. The blood glucose response area to potatoes with 100 g butter (448 +/- 68 mmol.240 min/L) was significantly lower than after the four other meals: 596 +/- 63 (potato alone), 649 +/- 82 (potato + 40 g olive oil), 587 +/- 80 (potato + 50 g butter), and 604 +/- 81 (potato + 80 g olive oil) nmol.240 min/L, P < 0.05, respectively. The insulin response was significantly increased by adding 50 and 100 g butter, whereas addition of 40 and 80 g olive oil had no effect. The fatty acid concentration was higher when 100 g butter was added to the potato meal than when it was not (0.67 +/- 0.05 compared with 0.48 +/- 0.07 mmol/L, P < 0.05). Fatty acid concentrations were similar to those found for the other meals. The triacylglycerol response increased in a dose-dependent manner with the fat content of the meals irrespective of the type of fat. We conclude that butter increases the insulin response more than does olive oil, and large amounts of butter also increase fatty acid and triacylglycerol concentrations.

The IGF system has been associated with development and progression of diabetic retinopathy. We examined whether a simple measurement of the IGF system (serum total IGF-I) correlated with progression of diabetic retinopathy in pregnancy in type 1 diabetes. A prospective observational study was performed in 103 pregnant women with type 1 diabetes. Serum IGF-I was measured in maternal serum from week 14, every fourth week until week 30, and every second week until delivery. Twenty-four-hour blood pressure was measured with a portable oscillometry monitor. The women had visual acuity testing and fundus photography before pregnancy, once in each trimester, and 4 months after birth. Each eye was assigned an overall retinopathy grade on a scale from 1 to 6 independently by two experienced graders. During pregnancy, serum IGF-I increased with increasing gestational age until a plateau was reached in week 32. Progression of retinopathy was significantly associated with a higher level of IGF-I (P < 0.01). Serum IGF-I increased with increasing progression of retinopathy. Change of retinopathy was significantly associated with level of IGF-I (P < 0.01). During pregnancy, serum IGF-I increased with increasing birth weight until a plateau was reached in week 32. Birth weight was significantly associated with a higher level of serum IGF-I (P < 0.01).