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1                                              GDM and HDP diagnoses were self-reported for each pregna
2                                              GDM increases the risk of long-term complications, inclu
3                                              GDM is currently the most common medical complication of
4                                              GDM may modulate both local and circulating levels of MM
5                                              GDM risk was significantly higher for APIs than whites f
6                                              GDM was associated with a series of retinal arteriolar a
7                                              GDM was diagnosed using the 2004 American Diabetes Assoc
8                                              GDM-exposed offspring of mothers with a protein intake i
9 Ws) 10-14, 15-26, 23-31, and 33-39 among 107 GDM cases (ascertained on average at GW 27) and 214 non-
10 thylation in placenta and cord blood from 27 GDM exposed and 21 unexposed offspring.
11  before and during pregnancy, 2) HDP, and 3) GDM.
12 reas in the standard care arm, there were 41 GDM and 160 1-h glucose-associated dmCpGs.
13                At gestational day (GD) 12.5, GDM produced a hyperglycemic, hyperleptinemic maternal s
14 pregnant women, 100 blood plasma samples (50 GDM and 50 healthy pregnant control group) were submitte
15 rnal preexisting type 2 diabetes (n = 6496), GDM diagnosed at 26 weeks' gestation or earlier (n = 745
16                                 In addition, GDM+MIA heightened the maternal inflammatory state and g
17               Lactation may prevent DM after GDM delivery.
18 ted with lower 2-year incidences of DM after GDM pregnancy.
19 iod via oral glucose tolerance testing after GDM, which is a time-consuming and inconvenient procedur
20 nt in maternal plasma of normal (n = 13) and GDM (n = 7) pregnancies.
21 ose mothers had both pregravid BMI >/=25 and GDM were at higher risk of an earlier transition to pubi
22  not modify the association between U-Cd and GDM (p = 0.26).
23 ysis was conducted on ECFCs from control and GDM pregnancies.
24  association between high PM2.5 exposure and GDM risk has not been well studied.
25 iation between MMPs concentration in GCF and GDM.
26 uggest an interaction between gingivitis and GDM.
27  available epidemiologic studies on iron and GDM.
28 ring pregnancy with blood glucose levels and GDM risk in Chinese women.
29 pregnancy increases blood glucose levels and GDM risk in Chinese women.
30 EVs as compared to sEVs from nonpregnant and GDM women.
31 diated by adrenomedullin (ADM) in normal and GDM pregnancies.
32 ncreased during gestation in both normal and GDM pregnancies; however, the increase was significantly
33 al glucose (75 g) tolerance test (OGTT), and GDM diagnosis was based on diagnostic criteria recommend
34 s from pregnant women with late-onset PE and GDM compared to controls.
35 ulated genes were found in late-onset PE and GDM placentas, which may suggest that these conditions c
36 ficant association between periodontitis and GDM in the meta-analyses of four cross-sectional studies
37 ng the association between periodontitis and GDM.
38 sitive association between periodontitis and GDM.
39 plasma of nonpregnant, healthy pregnant, and GDM women at 24-28 weeks of gestation.
40     Associations between total n-6 PUFAs and GDM were null, whereas associations with individual n-6
41                                      T2D and GDM also share common genetic architecture, but there ar
42 14, approximately 10-18 weeks earlier before GDM is typically screened for.
43      We investigated the association between GDM treatment and fetal, neonatal, and childhood growth.
44  suggested that a strong link exists between GDM and T2D.
45                       However, links between GDM and T2D are not well understood.
46 ic reduction on intragenic regions from both GDM and preeclampsia compared to healthy controls.
47 athers, with stronger associations when both GDM and GH were present.
48 offspring (HR, 1.21; 95% CI, 0.97-1.52), but GDM diagnosed at 26 weeks or earlier remained so (HR, 1.
49 ildren born after pregnancies complicated by GDM.
50     No genes were significantly regulated by GDM.
51                 We used a well-characterised GDM prospective cohort of 1035 women following up to 8 y
52              In order to better characterize GDM in pregnant women, 100 blood plasma samples (50 GDM
53 clusion, we found associations of a combined GDM/GH indicator with cardiometabolic disease in mothers
54                      We evaluated a combined GDM/GH risk indicator in both mothers and fathers becaus
55 is as a screening tool for fast and low-cost GDM detection.
56 Health Organization (WHO) criteria to define GDM: >/=7.0 mmol/L for fasting glucose and/or >/=7.8 mmo
57 n gene knockout mice (Adipoq (-/-) ) develop GDM due to insulin insufficiency.
58  a history of diabetes, 240 (7.1%) developed GDM.
59 use congenital hypothyroidism also developed GDM.
60                          Women who developed GDM showed increased concentrations of MMP-8 and -9 in G
61 11 years had a 51% higher risk of developing GDM (95% confidence interval: 1.10, 2.07) after adjustme
62  Treatment options for gestational diabetes (GDM) are limited.
63  years of mothers with gestational diabetes (GDM) in a cross-sectional study.
64 ely, 35% of women with Gestational Diabetes (GDM) progress to Type 2 Diabetes (T2D) within 10 years.
65 hild dyads affected by gestational diabetes (GDM).
66 of mothers with preexisting type 2 diabetes, GDM diagnosed at 26 weeks or earlier, GDM diagnosed afte
67 it from a maternal low protein intake as did GDM-exposed offspring.Overall, our results provide littl
68 didate gene for the study of gestational DM (GDM).
69         Although the role of exosomes during GDM remains to be fully elucidated, exosome profiles may
70 betes, GDM diagnosed at 26 weeks or earlier, GDM diagnosed after 26 weeks, and no diabetes, respectiv
71 rt of 1208 Chinese women who had experienced GDM.
72 eight reduction in women who had experienced GDM.
73 or earlier, and 0.98 (95% CI, 0.84-1.15) for GDM diagnosed after 26 weeks relative to no exposure.
74 per 1-kg/m(2) increase) were 32% and 22% for GDM and HDP, respectively.
75 ype 2 diabetes, 1.63 (95% CI, 1.35-1.97) for GDM diagnosed at 26 weeks or earlier, and 0.98 (95% CI,
76 e interval: 1.10, 2.07) after adjustment for GDM risk factors.
77 ing early pregnancy should be considered for GDM prevention.
78 ng, heterogeneity in diagnostic criteria for GDM, and the scarcity of reporting of childhood outcomes
79 s used, adjusting for major risk factors for GDM.
80           This makes them an ideal model for GDM.
81  between high ALT and overweight/obesity for GDM.
82 ogistic regression estimated odds ratios for GDM associated with high (>=75th percentile) versus low
83                              Odds ratios for GDM increased with increasing U-Cd tertile (OR = 1.64; 9
84 nd 11 (representing 6 cohorts and 1 RCT) for GDM.
85 ical activity are the primary treatments for GDM, but pharmacotherapy, usually insulin, is used when
86                       Exosomes isolated from GDM pregnancies significantly increased the release of p
87 urately distinguish risk of progression from GDM to T2D and that metabolite changes signify underlyin
88                  Mice infused with sEVs from GDM women developed glucose intolerance.
89 tance in nonpregnant mice and that sEVs from GDM women fail to stimulate insulin secretion and cause
90 lic signature predicting the transition from GDM to T2D in the early postpartum period that was super
91 st metabolomics study of the transition from GDM to T2D validated in an independent testing set, faci
92 ics signature to predict the transition from GDM to T2D.
93 the pathology underlying the transition from GDM to T2D.
94 thermore, 3'SL was more predictive of future GDM diagnoses than was fasting glucose in early pregnanc
95               Finally, 1332 (7.7%) women had GDM.
96 .40 SD; 95% CI: -0.03, 0.83 SD; P = 0.07) in GDM-exposed offspring and a tendency for a higher total
97  was 93 +/- 15 g/d (16% +/- 3% of energy) in GDM-exposed women and 90 +/- 14 g/d (16% +/- 2% of energ
98                PLAC8 was highly expressed in GDM-exposed ECFCs, and PLAC8 expression correlated with
99 r, the increase was significantly greater in GDM ( approximately 2.2-fold, approximately 1.5-fold, an
100 de heterogeneity in dosing, heterogeneity in GDM diagnostic criteria, and few studies reporting longi
101 ped for T2D to the study of heterogeneity in GDM.
102 pregnancy may improve glucose homeostasis in GDM-exposed and male offspring.
103 te the causal role of hypoadiponectinemia in GDM, adiponectin gene knockout (Adipoq(-/-) ) and wild-t
104                      While IR is impaired in GDM-placenta, it is unaffected in GDM-platelet.
105 nstream elements were significantly lower in GDM-trophoblast and showed no response to the insulin st
106                        Knockdown of PLAC8 in GDM-exposed ECFCs improved proliferation and senescence
107  findings with clinical samples show that in GDM-associated defect on IR is tissue type-dependent.
108 should be a leading factor for thrombosis in GDM maternal blood.
109 mpaired in GDM-placenta, it is unaffected in GDM-platelet.
110  prepregnancy Mediterranean diet on incident GDM and HDP and proportions mediated through prepregnanc
111  (1.31-2.00)] were associated with increased GDM risk.
112 tanding of environmental factors influencing GDM may facilitate early identification of women at high
113 tional diabetes mellitus (GDM), and 209 late GDM.
114 ancy was associated with substantially lower GDM risk.
115  2 diabetes mellitus and ethnicity are major GDM risk factors.
116                                     Maternal GDM, fasting glucose, 1-h, and 2-h glucose concentration
117 self-reported pregravid obesity and maternal GDM with timing of the daughter's transition to pubertal
118 osure to metformin for treatment of maternal GDM, neonates are significantly smaller than neonates wh
119 to 44 weeks' gestation, exposure to maternal GDM diagnosed by 26 weeks' gestation was associated with
120 anced electrocatalysts, gas diffusion media (GDM), ionomers, polymer electrolyte membranes (PEMs), an
121               Gestational diabetes mellitus (GDM) affects 3-14% of pregnancies, with 20-50% of these
122 ssociation of gestational diabetes mellitus (GDM) and gestational hypertension (GH) with cardiometabo
123 s and risk of gestational diabetes mellitus (GDM) and hypertensive disorders of pregnancy (HDP) remai
124 of women with gestational diabetes mellitus (GDM) and systemically healthy counterparts with differen
125 e in utero to gestational diabetes mellitus (GDM) and/or maternal immune activation (MIA).
126  a history of gestational diabetes mellitus (GDM) are at high risk of developing type 2 diabetes mell
127 psia (PE) and gestational diabetes mellitus (GDM) are common complications of pregnancy, but the mech
128 ncy (HDP) and gestational diabetes mellitus (GDM) are common maternal complications during pregnancy,
129 eclampsia and gestational diabetes mellitus (GDM) are the most common clinical conditions in pregnanc
130 prevalence of gestational diabetes mellitus (GDM) compared with other racial/ethnic groups.
131  a history of gestational diabetes mellitus (GDM) have a 7-fold higher risk of developing type 2 diab
132  treatment of gestational diabetes mellitus (GDM) in many countries.
133 odontitis and gestational diabetes mellitus (GDM) in the current literature.
134               Gestational diabetes mellitus (GDM) is a hyperglycaemic imbalance first recognized duri
135               Gestational diabetes mellitus (GDM) is conventionally confirmed with oral glucose toler
136               Gestational diabetes mellitus (GDM) is defined as varying glucose intolerance, with fir
137 tal growth in gestational diabetes mellitus (GDM) is directly linked to maternal glycaemic control; h
138 gy underlying gestational diabetes mellitus (GDM) is distinct from that underlying T2D.
139               Gestational diabetes mellitus (GDM) is increasing worldwide and women with a history of
140 evelopment of gestational diabetes mellitus (GDM) is largely unknown.
141 ion of Cd and gestational diabetes mellitus (GDM) is unknown.
142 gnancy and in gestational diabetes mellitus (GDM) remain poorly understood.
143 omplicated by gestational diabetes mellitus (GDM) remains to be established.
144 us (DM) after gestational diabetes mellitus (GDM) remains uncertain.
145               Gestational diabetes mellitus (GDM) shares phenotypic characteristics with T2D.
146 evelopment of gestational diabetes mellitus (GDM) that included fasting glucose, prepregnancy BMI, ge
147 s, even below gestational diabetes mellitus (GDM) thresholds, are associated with adverse offspring o
148 besity and/or gestational diabetes mellitus (GDM) was associated with early puberty in girls.
149 evelopment of gestational diabetes mellitus (GDM), a common pregnancy complication which has short-te
150 ation between gestational diabetes mellitus (GDM), a state of transient hyperglycemia during pregnanc
151 tes, 95 early gestational diabetes mellitus (GDM), and 209 late GDM.
152 nce (IGT) and gestational diabetes mellitus (GDM), and we used linear regression models to estimate a
153 ls results in gestational diabetes mellitus (GDM), reduced beta-cell proliferation, and failure to ex
154 ) and risk of gestational diabetes mellitus (GDM), while the association between high PM2.5 exposure
155 oblast of the gestational diabetes mellitus (GDM)-associated placenta, SERT is found entrapped in the
156 en with prior gestational diabetes mellitus (GDM).
157 en with prior gestational diabetes mellitus (GDM).
158 patients with gestational diabetes mellitus (GDM).
159  menarche and gestational diabetes mellitus (GDM).
160 also predicts gestational diabetes mellitus (GDM).
161 s involved in gestational diabetes mellitus (GDM).
162 isk factor of gestational diabetes mellitus (GDM).
163 xacerbated by gestational diabetes mellitus (GDM).
164 quent risk of gestational diabetes mellitus (GDM).
165 gnancies with gestational diabetes mellitus (GDM).Six hundred eight women with an index pregnancy aff
166 to women with gestational diabetes mellitus (GDM).The analysis included 918 mother-singleton child dy
167 duced risk of gestational diabetes mellitus (GDM); however, the association of composite healthy life
168 iagnosis of 'gestational diabetes mellitus' (GDM) and thus treatment during pregnancy.
169 lymers based on the Gaussian disorder model (GDM) for site energies while employing Pauli's master eq
170                 Compared with having neither GDM nor GH, having either was associated with incident d
171 ancy; in the intervention arm, there were no GDM and two 1-h glucose-associated dmCpGs, whereas in th
172 ascertained on average at GW 27) and 214 non-GDM controls.
173 tric indices were higher in the GDM than non-GDM group (P <0.0001).
174  glucose was significantly higher for both O-GDM and O-T1D compared with O-BP (P < 0.05).
175 C1A gene expression in muscle was lower in O-GDM compared with O-BP (P = 0.0003), whereas no differen
176 te to the decreased PPARGC1A expression in O-GDM.
177 the increased risk of metabolic disease in O-GDM.
178  women with gestational diabetes mellitus (O-GDM) or type 1 diabetes (O-T1D) and of women from the ba
179 l recent studies have reported an absence of GDM phenotype in their colony.
180 EV content contributes to the development of GDM.
181  early to midpregnancy in the development of GDM.
182                         A first diagnosis of GDM was reported by 357 women (7.5%).
183 ADPSG), with 159 women having a diagnosis of GDM.
184 easing worldwide and women with a history of GDM are at risk of developing type 2 diabetes which is a
185         Among Danish women with a history of GDM, ASB intake was not significantly associated with ca
186 ter age at childbearing, previous history of GDM, family history of type 2 diabetes mellitus and ethn
187                   In women with a history of GDM, greater intakes of total iron, dietary heme iron, a
188 s data further validates our animal model of GDM and is usefulness in investigating the pathophysiolo
189 hers do not use the db/+ mouse as a model of GDM unless they are certain the phenotype remains in the
190     Previously we developed a mouse model of GDM, however we did not evaluate alterations to energy a
191 ove treatments, appropriate animal models of GDM are crucial.
192 levels was associated with increased odds of GDM among whites and APIs.
193 nfidence interval: 12, 47) increased odds of GDM among whites compared with 45% (95% confidence inter
194 d 23% (95% CI: 1.01, 1.50) increased odds of GDM during trimester 1 and trimester 2, respectively.
195                                  Outcomes of GDM-affected pregnancies randomised to treatment with me
196                                  Outcomes of GDM-affected pregnancies randomised to treatment with me
197 ar, may be implicated in the pathogenesis of GDM, with significant associations and incremental predi
198 ness in investigating the pathophysiology of GDM.
199 al-age profile of PdEs in maternal plasma of GDM with normal pregnancies and to determine the effect
200 o suggest a beneficial role in prevention of GDM, although not excluding the potential benefit of EPA
201 timulation up-regulated 5-HT uptake rates of GDM-platelets as it does in the control group.
202          Similarly, the 5-HT uptake rates of GDM-trophoblast and the SERT expression on their surface
203 core was associated with a 21% lower risk of GDM (95% confidence interval: 0.65, 0.96) after adjustme
204 a 45% (0.55; 95% CI 0.37-0.83) lower risk of GDM (all FDR-corrected P values < 0.05).
205 dels were used to determine relative risk of GDM (n = 140 cases) in relation to healthy lifestyle.
206 nean diet was associated with higher risk of GDM (OR: 1.35; 95% CI: 1.02, 1.60) and HDP (OR: 1.41; 95
207 ere related to a substantially lower risk of GDM (ORQ4-Q1 0.04 [0.01, 0.06]).
208 valuate available data examining the risk of GDM associated with dietary iron, iron supplementation,
209 th the periodontal diagnosis and the risk of GDM development.
210 est that body burden of Cd increases risk of GDM in a dose-dependent manner.
211 CI 0.14-0.95; P value = 0.039) lower risk of GDM versus women with low n-3 and high n-6 PUFAs.
212 ; 95% CI 0.45-0.99; P = 0.047) lower risk of GDM, respectively; however, the significance did not per
213 ted with a 1.40- to 1.95-fold higher risk of GDM, whereas docosatetraenoic acid (DTA) at GW 15-26 was
214 enarche may identify women at higher risk of GDM.
215 arly identification of women at high risk of GDM.
216 ol to identify women at high and low risk of GDM.
217 ietary patterns during pregnancy and risk of GDM.
218 er gestational window in relation to risk of GDM.
219 regnancy are associated with reduced risk of GDM.
220 ictive models, capturing the future risks of GDM in the temporally aggregated EHRs.
221 r further adjusting for traditional risks of GDM, arteriolar branching angle remained significantly l
222 sidered as a candidate gene for the study of GDM.
223 ype- and genotype-based subclassification of GDM to deliver the promise of precision medicine to the
224 nificantly altered in the umbilical veins of GDM and preeclampsia.
225  of 64,232 couples were categorized based on GDM/GH status (neither, either, or both).
226 ts of the prepregnancy Mediterranean diet on GDM and HDP risk.
227                           Increased focus on GDM risk in US API communities is warranted.
228 During 12 years of follow-up, information on GDM diagnosis was obtained for each live birth.
229  and clinical periodontal parameters in only GDM group.
230  were exposed to either vehicle, GDM, MIA or GDM+MIA.
231 ) evaluate energy and fat homeostasis in our GDM mouse model and (2) determine if ADM may play a role
232 ated genes in placental biopsies between PE, GDM, or uncomplicated pregnancy (n = 10 each group).
233 machine learning models with EHRs to predict GDM, which will facilitate personalized medicine in mate
234 trimester even within normal range predicted GDM risk, further enhanced by overweight/obesity.
235 eletion in maternal beta-cells also produced GDM, with inadequate beta-cell expansion accompanied by
236                       The most significantly GDM-associated CpG was cg03566881 located within the leu
237  exposures in age at menarche and subsequent GDM risk.
238 ly-to-midpregnancy in relation to subsequent GDM risk in a case-control study of 107 case subjects wi
239                         However, unlike T2D, GDM emerges in the setting of profound pregnancy-related
240 higher in the GDM with gingivitis group than GDM without gingivitis group.
241 ere, we investigated a novel hypothesis that GDM-associated defects in platelet IR should change thei
242 In conclusion, we were unable to acquire the GDM phenotype in any of our experiments, and we recommen
243 ned at the time of cesarean section from the GDM and non-diabetic subjects (n = 6 for each group), an
244  and saliva sRANKL levels were higher in the GDM group (P <0.05).
245 nd anthropometric indices were higher in the GDM than non-GDM group (P <0.0001).
246 saliva sRANKL (P <0.0001) were higher in the GDM with gingivitis group than GDM without gingivitis gr
247                        A total of 87% of the GDM and 77% of the 1-h glucose-associated dmCpGs had sma
248 T is found entrapped in the cytoplasm of the GDM-trophoblast.
249                   Moreover, we show that the GDM and 1-h glucose-associated methylation signatures in
250 severe periodontitis and associated with the GDM development.
251 pidemia during the early postpartum in those GDM women who progress to T2D and suggest endogenous lip
252 e data, we hypothesize that children born to GDM mothers and exposed to midgestation infections have
253 isk of hyperglycemia among offspring born to GDM mothers in Tianjin, China.
254 nancy glycemic regulation that contribute to GDM.
255 xposed to GDM at </=26 weeks, 180 exposed to GDM at >26 weeks, and 2963 unexposed).
256  preexisting type 2 diabetes, 130 exposed to GDM at </=26 weeks, 180 exposed to GDM at >26 weeks, and
257 rming cells (ECFCs) from neonates exposed to GDM exhibit impaired function.
258 enetic and physiologic pathways that lead to GDM differ, at least in part, from those that lead to T2
259 and maternal glycaemic control when treating GDM.
260  Ontology analysis using loci bearing unique GDM- and preeclampsia-specific loss-of-5hmC indicated it
261 mouse brains were exposed to either vehicle, GDM, MIA or GDM+MIA.
262 P-8 concentration in GCF was associated with GDM (RR: 1.19; P = 0.045; CI 95% 1.00 to 1.40; and RR: 1
263  a cluster that was strongly associated with GDM as well as associated with higher infant birth weigh
264   ALT levels were positively associated with GDM risk without a clear threshold.
265 GF-I/IGFBP-3 were positively associated with GDM risk; adjusted odds ratio (OR) comparing the highest
266  groups of maternal variants associated with GDM using two complementary approaches that were based o
267 epatic lipid metabolism were associated with GDM; these clusters were not associated with infant birt
268 ect size for this cluster's association with GDM appeared greater than that for T2D.
269 gy outside of pregnancy for association with GDM.
270 d tested these clusters for association with GDM.
271             PFOS and PFHxS associations with GDM (53 cases) were in a similar direction, but less pre
272  for the association of LGR6 cg03566881 with GDM was 0.317 (95% confidence interval (CI) 0.012, 0.022
273 T) was identified in a female diagnosed with GDM and GTD as well as in her father with type 2 DM but
274 research study of 1,035 women diagnosed with GDM.
275 rcent of the pregnancies were diagnosed with GDM.
276                  There were 101 females with GDM and 66 females without GDM.
277 iveness were attenuated in mice infused with GDM sEVs.
278 l-range risk associations of ALT levels with GDM.
279 hnicity and maternal education, mothers with GDM had narrower arteriolar caliber (-1.6 mum; 95% Confi
280  identified in matched pairs of mothers with GDM or without GDM (matched on age group, health region,
281 emained significantly larger in mothers with GDM than those without GDM (2.0 degrees ; 95% CI: 0.5 de
282          PAX8 was genotyped in patients with GDM and gestational thyroid dysfunction (GTD), a patholo
283 site healthy lifestyle during pregnancy with GDM has not been examined.
284 case-control study of 107 case subjects with GDM and 214 control subjects without GDM, with blood sam
285                       Seventy-one women with GDM and gingivitis (Gg), 30 women with GDM and healthy p
286  with GDM and gingivitis (Gg), 30 women with GDM and healthy periodontium (Gh), 28 systemically and p
287 ecommended, but fewer than 40% of women with GDM are tested.
288                   We included 607 women with GDM from the Danish National Birth Cohort (DNBC; 1996-20
289   Magnesium supplementation among women with GDM had beneficial effects on metabolic status and pregn
290 n with available HbA(1c)) and for women with GDM only.
291     A prospective cohort of 1,035 women with GDM pregnancy were enrolled at 6-9 weeks postpartum (bas
292 ndependent longitudinal cohort of women with GDM who had glucose tolerance tested during the early po
293                     Among 110,879 women with GDM, 9173 women (8.3%) were treated with glyburide (n =
294 eceding progression to T2D, among women with GDM.
295 m offspring born to mothers with and without GDM.
296  101 females with GDM and 66 females without GDM.
297 degrees , 3.3 degrees ) than mothers without GDM.
298 matched pairs of mothers with GDM or without GDM (matched on age group, health region, and year of de
299 ts with GDM and 214 control subjects without GDM, with blood sample collection at gestational weeks 1
300 arger in mothers with GDM than those without GDM (2.0 degrees ; 95% CI: 0.5 degrees , 3.6 degrees ).

 
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