Urinary C-Peptide in the Neonate Correlates Both to Maternal Glucose Tolerance and to Fetal Size at Birth

1988 ◽  
Vol 5 (02) ◽  
pp. 144-145 ◽  
Author(s):  
N-O. Lunell ◽  
B. Persson ◽  
L. Devarajan ◽  
S. Hassan ◽  
H. Hathout ◽  
...  
1996 ◽  
Vol 270 (6) ◽  
pp. R1371-R1379 ◽  
Author(s):  
K. L. Teff ◽  
K. Engelman

In animals, bypassing the oropharyngeal receptors by intragastric administration of glucose results in glucose intolerance. To determine whether the absence of oral sensory stimulation alters glucose tolerance in humans, we monitored plasma levels of glucose and hormones after intragastric administration of glucose, with and without subjects tasting food. Plasma glucose area under the curve (AUC) was significantly lower after oral sensory stimulation (3,433 +/- 783 vs. 5,643 +/- 1,397 mg.dl-1. 195 min-1; P < 0.03; n = 8). Insulin and C-peptide AUCs were higher during the first one-half of the sampling period (insulin, 5,771 +/- 910 vs. 4,295 +/- 712 microU. ml-1.75 min-1; P < 0.05; C-peptide, 86 +/- 10 vs. 66 +/- 9 ng.ml-1. 75 min-1; P < 0.03) and lower during the second one-half of the sampling period compared with the control condition (1,010 +/- 233 vs. 2,106 microU.ml-1. 120 min-1; P < 0.025; 31 +/- 8 vs. 56 +/- 18 ng.ml-1. 120 min-1; P < 0.05; insulin and C-peptide, respectively). Oral sensory stimulation markedly increased plasma glucagon compared with the control condition (1,258 +/- 621 vs. -2,181 +/- 522 pg.ml-1. 195 min-1; P < 0.002). These data provide evidence in humans that oral sensory stimulation influences glucose metabolism and suggest that the mechanisms elicited by this cephalic stimulation are necessary for normal glucose homeostasis.


Author(s):  
Jan Farrell ◽  
Jill M. Forrest ◽  
G. N. Bruce Storey ◽  
D. K. Yue ◽  
R. P. Shearman ◽  
...  

2021 ◽  
Author(s):  
Jami L. Josefson ◽  
Denise M. Scholtens ◽  
Alan Kuang ◽  
Patrick M. Catalano ◽  
Lynn P. Lowe ◽  
...  

<b>OBJECTIVE</b> <p>Excessive childhood adiposity is a risk factor for adverse metabolic health. The objective was to investigate associations of newborn body composition and cord C-peptide with childhood anthropometrics and explore whether these newborn measures mediate associations of maternal mid-pregnancy glucose and BMI with childhood adiposity.</p> <p><b>RESEARCH DESIGN AND METHODS</b></p> <p>Data on mother/offspring pairs (N=4832) from the epidemiological Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study and HAPO Follow Up Study (HAPO FUS) were analyzed. Linear regression was used to study associations between newborn and childhood anthropometrics. Structural equation modeling was used to explore newborn anthropometric measures as potential mediators of the associations of maternal BMI and glucose during pregnancy with childhood anthropometric outcomes. </p> <p><b>RESULTS</b></p> <p>In models including maternal glucose and BMI adjustments, newborn adiposity as measured by sum of skinfolds was associated with child outcomes (adjusted mean difference, 95% CI, p-value) BMI(0.26,0.12-0.39,<0.001), BMI z-score(0.072,0.033-0.11,<0.001), fat mass (kg)(0.51,0.26-0.76,<0.001), percent bodyfat(0.61, 0.27-0.95,<0.001), and sum of skinfolds (mm)(1.14,0.43-1.86,0.0017). Structural equation models demonstrated significant mediation by newborn sum of skinfolds and cord C-peptide of maternal BMI effects on childhood BMI(proportion of total effect 2.5% and 1%, respectively), fat mass(3.1%,1.2%), percent bodyfat(3.6%,1.8%), and sum of skinfolds (2.9%,1.8%), and significant mediation by newborn sum of skinfolds and cord C-peptide of maternal glucose effects on child fat mass (proportion of total association 22.0% and 21.0%, respectively), percent bodyfat (15.0%,18.0%), and sum of skinfolds (15.0%,20.0%).</p> <p><b>CONCLUSIONS</b></p> <p>Newborn adiposity is independently associated with childhood adiposity and, along with fetal hyperinsulinemia, mediates, in part, associations of maternal glucose and BMI with childhood adiposity. </p>


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Samantha M. McDonald ◽  
Linda E. May ◽  
Stefanie N. Hinkle ◽  
Katherine L. Grantz ◽  
Cuilin Zhang

2020 ◽  
Vol 105 (10) ◽  
pp. 3179-3189
Author(s):  
Marissa J Kilberg ◽  
Clea Harris ◽  
Saba Sheikh ◽  
Darko Stefanovski ◽  
Marina Cuchel ◽  
...  

Abstract Context Oral glucose tolerance test (OGTT)-related hypoglycemia is common in pancreatic-insufficient cystic fibrosis (PI-CF), but its mechanistic underpinnings are yet to be established. Objective To delineate the mechanism(s) underlying OGTT-related hypoglycemia. Design and Setting We performed 180-minute OGTTs with frequent blood sampling in adolescents and young adults with PI-CF and compared results with those from a historical healthy control group. Hypoglycemia (Hypo[+]) was defined as plasma glucose &lt;65 mg/dL. We hypothesized that CF-Hypo[+] would demonstrate impaired early phase insulin secretion and persistent late insulin effect compared with control-Hypo[+], and explored the contextual counterregulatory response. Main Outcome Measure OGTT 1-hour and nadir glucose, insulin, C-peptide, and insulin secretory rate (ISR) incremental areas under the curve (AUC) between 0 and 30 minutes (early) and between 120 and 180 minutes (late), and Δglucagon120-180min and Δfree fatty acids (FFAs)120-180min were compared between individuals with CF and control participants with Hypo[+]. Results Hypoglycemia occurred in 15/23 (65%) patients with CF (43% female, aged 24.8 [14.6-30.6] years) and 8/15 (55%) control participants (33% female, aged 26 [21-38] years). The CF-Hypo[+] group versus the control-Hypo[+] group had higher 1-hour glucose (197 ± 49 vs 139 ± 53 mg/dL; P = 0.05) and lower nadir glucose levels (48 ± 7 vs 59 ± 4 mg/dL; P &lt; 0.01), while insulin, C-peptide, and ISR-AUC0-30 min results were lower and insulin and C-peptide, and AUC120-180min results were higher (P &lt; 0.05). Individuals with CF-Hypo[+] had lower Δglucagon120-180min and ΔFFA120-180min compared with the control-Hypo[+] group (P &lt; 0.01). Conclusions OGTT-related hypoglycemia in PI-CF is associated with elevated 1-hour glucose, impaired early phase insulin secretion, higher late insulin exposure, and less increase in glucagon and FFAs. These data suggest that hypoglycemia in CF is a manifestation of islet dysfunction including an impaired counterregulatory response.


1996 ◽  
Vol 5 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Katsuyuki Miura ◽  
Hideaki Nakagawa ◽  
Muneko Nishijo ◽  
Masaji Tabata ◽  
Yuko Morikawa ◽  
...  

2019 ◽  
Vol 20 (4) ◽  
pp. 408-413
Author(s):  
Heba M. Ismail ◽  
Carmella Evans‐Molina ◽  
Linda A. DiMeglio ◽  
Dorothy J. Becker ◽  
Ingrid Libman ◽  
...  

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