No association of natural killer cell number and function in peripheral blood with overweight/obesity and metabolic syndrome in a cohort of young women.

AIM: To reexamine the associations of NK cell number and function in the peripheral blood with overweight/obesity and the metabolic syndrome in a large, well-phenotyped human cohort. METHODS: Cross-sectional analysis of 273 women in the PPSDiab Study; measurement of absolute and relative number of NK cells in peripheral blood, and of functional parameters CD69 positivity and cytotoxicity against K562 cells; group comparison of NK cell characteristics between lean, overweight, and obese participants, as well as metabolic syndrome scores of 0, 1, 2, and ≥3; Spearman correlation analyses to clinical parameters related to the metabolic syndrome. RESULTS: We found no differences in NK cell number and function between lean, overweight, and obese women (relative NK cell number (median (Q1-Q3), [%]) 5.1(2.6-9.4) vs. 4.8 (2.9-8.4) vs. 3.8 (1.7-7.8), p = 0.187; absolute NK cell number [106 /L]: 86.9 (44.6-188.8) vs. 92.6 (52.5-154.6) vs. 85.9 (44-153.8), p = 0.632; CD69+ [%]: 27.2 (12.9-44.3) vs. 37.6 (13.2-52.8) vs. 33.6 (16.3-45), p = 0.136; cytotoxicity [%]: 11.0 (7.1-14.5) vs. 8.5 (6.4-13.2) vs. 11.3 (8.7-14.2), p = 0.094), as well as between different metabolic syndrome scores. Nonesterified fatty acids correlated with absolute and relative NK cell number and cytotoxicity (ρ [p-value]: 0.142 [0.021], 0.119 [0.049], and 0.131 [0.035], respectively). Relative NK cell number further correlated with high-density lipoprotein cholesterol (0.144 [0.018]) and cytotoxicity with 2 h glucose in oral glucose tolerance testing (0.132 [0.034]). CD69 positivity correlated with body fat (0.141 [0.021]), triglycerides (0.129 [0.033]), and plasma leptin (0.155 [0.010]). After correction for multiple testing, none of the associations remained significant. CONCLUSION: In the present study, we observed no associations of NK cell number and function in the peripheral blood with overweight/obesity and the metabolic syndrome. Extreme phenotypes of obesity and the metabolic syndrome might have caused differing results in previous studies. Further analyses with a focus on compartments other than peripheral blood may help to clarify the relation between NK cells and metabolic diseases.

No deleterious effect of an additional pregnancy on glucose metabolism in women with previous gestational diabetes mellitus.

OBJECTIVE: Women with gestational diabetes mellitus (GDM) often develop type 2 diabetes later in life. It remains unclear whether this results solely from a common underlying predisposition or, whether a pregnancy itself persistently impairs glucose metabolism in predisposed women. We therefore examined how an additional pregnancy affected different aspects of glucose metabolism in women with previous GDM. RESEARCH DESIGN AND METHODS: Nested case-control study within the prospective cohort study PPSDiab, recruited in Munich, Germany from 2011-16. Cases (n = 41): women with previous GDM who completed an additional pregnancy; controls: no additional pregnancy, pairwise matching. ENDPOINTS: change of the area under the glucose curve (AUGC) of an oral glucose tolerance, of plasma glucose at 60' of the test (PG 60'), of the insulin sensitivity index (ISI) and of the disposition index (DI), all between before and after the additional pregnancy in cases/the corresponding observation period in controls. RESULTS: We observed no significant difference between cases and controls in the primary [ratio AUGC 1.05(0.92-1.15) vs. 0.97(0.85-1.14); p = 0.21] and in the secondary endpoints [difference PG 60', ratio ISI and ratio DI. CONCLUSION: We did not find a deleterious effect of an additional pregnancy on glucose metabolism in women with previous GDM.