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OBJECTIVE -To study the relationship between low birth weight and the presence of gestational diabetes mellitus (GDM) or peripheral insulin resistance during pregnancy.RESEARCH DESIGN AND METHODS -We studied the relationship between peripheral insulin sensitivity (calculated by Matsuda and DeFronzo's oral glucose tolerance test (OGTT)-derived insulin sensitivity index [ISI OGTT ]) or GDM prevalence and birth weight in 604 pregnant women, classified as normally glucose tolerant (n ϭ 462) or affected with GDM (n ϭ 142) after a 100-g 3-h oral glucose tolerance test. We then categorized these subjects into two groups: individuals with birth weight in the Ͻ10th percentile (Ͻ2,600 g; n ϭ 68) and individuals with birth weight in the Ͼ10th percentile (n ϭ 536).RESULTS -GDM prevalence was higher in the group in the lowest birth weight decile (Ͻ2,600 g; 24/68; 35%) than in the group with normal/high birth weight (118/536; 22%; 2 ϭ 5.917; P ϭ 0.01). Relative risk for GDM adjusted for age, parity, family history of diabetes, and prepregnancy body weight was about twofold in the group with low birth weight (odds ratio ϭ 1.89 [95% CI 1.088 -3.285; P ϭ 0.023]), and the prevalence of low birth weight was about threefold higher in the first ISI OGTT decile. In 450 women whose newborn's weight was known, the delivery of macrosomic babies was associated with a twofold higher relative risk for GDM in women who themselves had low birth weight. In the latter, the relationships between their newborn's weight and either maternal glucose tolerance (positive) or ISI OGTT (negative) were amplified.CONCLUSIONS -Low maternal birth weight was associated with a twofold higher risk for GDM, independent of major confounders. Such a risk was highest in women with low birth weight who delivered macrosomic babies, and in the group with low birth weight, the relationship between maternal glucose tolerance or insulin resistance and offspring's neonatal weight was much more evident.

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Viruses may cause Type 1 (insulin-dependent) diabetes. We wondered whether the number and function of natural killer cells, which are important in anti-viral defense, are disturbed in diabetic patients. We studied 16 recently diagnosed Type 1 diabetic patients, 18 Type 1 diabetic patients diagnosed more than 15 years previously, 18 Type 2 (non-insulin-dependent) diabetic patients and 23 control subjects. We determined the number of natural killer cells (expressed as log10%) using anti-Leu 11 monoclonal antibody and the function (in log10 lytic units) concurrently using a 51Cr release assay with K562 as target cells. We found that the number of natural killer cells was reduced in Type 1 diabetes (1.01 +/- 0.04) as compared with Type 2 diabetic patients (1.16 +/- 0.04, p = 0.004) and normal control subjects (1.16 +/- 0.04, p = 0.006). To establish whether the reduced natural killer cell number is genetically determined we studied 19 identical twin pairs discordant for Type 1 diabetes; we found that even the non-diabetic co-twins had a reduced natural killer cell number (0.93 +/- 0.05, p = 0.0006) as compared with normal control subjects. Natural killer cell function was similar in all groups while natural killer activity per cell was significantly increased in the recently diagnosed diabetic patients (1.63 +/- 0.07) as compared with long-standing diabetic patients (1.26 +/- 0.26, p = 0.03) and controls subjects (1.36 +/- 0.07, p = 0.006). In conclusion the reduced number of natural killer cells in Type 1 diabetes appears to be genetically determined while their activity at diagnosis is increased.