scholarly journals Postnatal insulin secretion and sensitivity after manipulation of fetal growth by embryo transfer in the horse

2004 ◽  
Vol 181 (3) ◽  
pp. 459-467 ◽  
Author(s):  
AJ Forhead ◽  
JC Ousey ◽  
WR Allen ◽  
AL Fowden
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Embryo Transfer ◽  
Plasma Glucose ◽  
Cell Function ◽  
The Other ◽  
Intrauterine Growth ◽  
Cell Responses ◽  
The Relationship

This study examined the effects of intrauterine growth on insulin secretion and resistance in newborn foals. Embryo transfer between small pony and large Thoroughbred mares was used to produce four groups of foals with different birth weights (pony in pony n=7; pony in Thoroughbred n=7; Thoroughbred in Thoroughbred n=8; Thoroughbred in pony n=8). On day 2 after birth, glucose (0.5 g/kg) was administered intravenously to the foal and blood samples were taken for 2 h to determine plasma glucose and insulin concentrations. On day 3, insulin sensitivity was assessed by giving insulin (0.75 U/kg i.v.) and measuring the decrement in plasma glucose in the foals. There were no significant differences in insulin secretion, insulin sensitivity or glucose tolerance between the control and growth-retarded Thoroughbred foals. Overgrown pony foals delivered by Thoroughbred mares had higher basal insulin levels and greater beta cell responses to glucose than the other groups of foals. The relationship between plasma glucose and insulin was also significantly steeper in overgrown pony foals than in the other groups. Variations in intrauterine growth rate, therefore, affect postnatal insulin secretion in the horse. More specifically, it is overgrowth, not growth retardation in utero that alters equine beta cell function in the immediate neonatal period.

Quantification of the relationship between insulin sensitivity and beta-cell function in human subjects. Evidence for a hyperbolic function

Diabetes ◽  
1993 ◽  
Vol 42 (11) ◽  
pp. 1663-1672 ◽  
Author(s):  
S. E. Kahn ◽  
R. L. Prigeon ◽  
D. K. McCulloch ◽  
E. J. Boyko ◽  
R. N. Bergman ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Human Subjects ◽  
Hyperbolic Function ◽  
The Relationship

scholarly journals The Relationship between Serum 25-Hydroxy Vitamin D and Insulin Sensitivity and  β-Cell Function in Newly Diagnosed Type 2 Diabetes

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Yuan Gao ◽  
Xinchi Wu ◽  
Qi Fu ◽  
Yanyun Li ◽  
Tao Yang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Vitamin D ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Newly Diagnosed ◽  
25 Hydroxy Vitamin D ◽  
The Relationship ◽  
Diabetes Patients

The aim of this study was to investigate the relationship between serum 25-hydroxy vitamin D (25-OHD) and insulin sensitivity andβ-cell function in newly diagnosed type 2 diabetes. 395 newly diagnosed type 2 diabetes patients were enrolled in this study. Venous blood samples were collected at 0 min, 30 min, and 120 min of OGTT to measure serum glucose and insulin. Matsuda ISI and HOMA-IR were used to determine insulin sensitivity. The ratio of 0–120 min area under curve of insulin to glucose (insulin release index, INSR) was calculated as surrogate index ofβ-cell insulin secretion function. The products of insulin secretion indices multiplied by Matsuda insulin sensitivity index were used as disposition indices. Patients were divided into three groups according to tertiles (T1, T2, and T3) of 25-OHD concentration. There was significant difference among three groups for HOMA-IR, Matsuda ISI, and INSR. HOMA-IR, Matsuda ISI, INSR, and DI were undifferentiated among three groups in male patients. But HOMA-IR, Matsuda ISI, and INSR were significantly different among three groups in female patients after being adjusted by confounding factors. In conclusion, serum 25-OHD is associated with insulin sensitivity andβ-cell function for female newly diagnosed type 2 diabetes patients, and the association is ambiguous in males.

scholarly journals Importance of quantifying insulin secretion in relation to insulin sensitivity to accurately assess beta cell function in clinical studies

2004 ◽  
pp. 97-104 ◽  
Author(s):  
B Ahren ◽  
G Pacini
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Glucose Tolerance Test ◽  
Cell Function ◽  
Tolerance Test ◽  
Hyperbolic Function

Insulin sensitivity and insulin secretion are mutually related such that insulin resistance is compensated by increased insulin secretion. A correct judgement of insulin secretion therefore requires validation in relation to the insulin sensitivity in the same subject. Mathematical analyses of the relationship between insulin sensitivity and insulin secretion has revealed a hyperbolic function, such that the product of the two variables is constant. This product is usually called the disposition index. Several techniques may be used for its estimation such as data derived from the frequently sampled i.v. glucose tolerance test, the oral glucose tolerance test or the glucose-dependent arginine stimulation test or the euglycemic hyperinsulinemic clamp technique in combination with a test on insulin secretion. Using these techniques the compensatory increase in beta cell function in insulin resistance has been verified in obesity, in pregnancy and after glucocorticoid administration as has the defective beta cell function as the underlying cause of impaired glucose tolerance and type 2 diabetes. Similarly, combined analysis of insulin sensitivity and insulin secretion has shown a down-regulation of beta cell function in increased insulin sensitivity accompanying weight reduction in obesity and following exercise. Acknowledging this inverse relationship between insulin secretion and insulin sensitivity therefore requires estimation of both variables for correct assessment in any individual.

scholarly journals Ethnic differences in beta cell function occur independently of insulin sensitivity and pancreatic fat in black and white men

2021 ◽  
Vol 9 (1) ◽  
pp. e002034
Author(s):  
Meera Ladwa ◽  
Oluwatoyosi Bello ◽  
Olah Hakim ◽  
Fariba Shojaee-Moradie ◽  
Maria Linda Boselli ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Ethnic Differences ◽  
Beta Cell Function ◽  
Cell Function ◽  
White Men ◽  
Black And White ◽  
Pancreatic Fat ◽  
Postprandial Insulin

IntroductionIt is increasingly recognized that type 2 diabetes (T2D) is a heterogenous disease with ethnic variations. Differences in insulin secretion, insulin resistance and ectopic fat are thought to contribute to these variations. Therefore, we aimed to compare postprandial insulin secretion and the relationships between insulin secretion, insulin sensitivity and pancreatic fat in men of black West African (BA) and white European (WE) ancestry.Research design and methodsA cross-sectional, observational study in which 23 WE and 23 BA men with normal glucose tolerance, matched for body mass index, underwent a mixed meal tolerance test with C peptide modeling to measure beta cell insulin secretion, an MRI to quantify intrapancreatic lipid (IPL), and a hyperinsulinemic-euglycemic clamp to measure whole-body insulin sensitivity.ResultsPostprandial insulin secretion was lower in BA versus WE men following adjustment for insulin sensitivity (estimated marginal means, BA vs WE: 40.5 (95% CI 31.8 to 49.2) × 103 vs 56.4 (95% CI 48.9 to 63.8) × 103 pmol/m2 body surface area × 180 min, p=0.008). There was a significantly different relationship by ethnicity between IPL and insulin secretion, with a stronger relationship in WE than in BA (r=0.59 vs r=0.39, interaction p=0.036); however, IPL was not a predictor of insulin secretion in either ethnic group following adjustment for insulin sensitivity.ConclusionsEthnicity is an independent determinant of beta cell function in black and white men. In response to a meal, healthy BA men exhibit lower insulin secretion compared with their WE counterparts for their given insulin sensitivity. Ethnic differences in beta cell function may contribute to the greater risk of T2D in populations of African ancestry.

scholarly journals A reduced incretin effect mediated by the rs7903146 variant in the TCF7L2 Gene is an early marker of beta-cell dysfunction in obese youth

2020 ◽  
Author(s):  
Alfonso Galderisi ◽  
Domenico Trico ◽  
Bridget Pierpont ◽  
Veronika Shabanova ◽  
Stephanie Samuels ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Plasma Glucose ◽  
Metabolic Phenotype ◽  
Glucose Disposal ◽  
Incretin Effect ◽  
Tcf7l2 Gene ◽  
Intravenous Glucose ◽  
Hyperglycemic Clamp

<b>Background.</b> The risk genotype for the common variant <i>rs7903146 </i>of the transcription factor-7-like-2 gene (<i>TCF7L2</i>) has been found to affect the incretin response in healthy and obese adults, however, whether a similar functional defect is also present in obese adolescents remains unexplored. Herein, we examined the functional effect of the <i>rs7903146</i> variant in the TCF7L2 gene on the incretin effect and determined its translational metabolic manifestation by performing deep phenotyping of the incretin system, beta-cell function relative to insulin sensitivity, the Gastrointestinal Induced Glucose Disposal (GIGD) in obese youths with normal and impaired glucose tolerance. <p><b>Methods</b> Thirty nine non-diabetic obese adolescents (15[14,18] years; BMI 37[33, 43]kg/m<sup>2</sup>) were genotyped for the <i>rs7903146 </i>of <i>TCF7L2</i> and underwent a 3-hour OGTT followed by an iso-glycemic intravenous glucose infusion (iso-IVGTT) to match the plasma glucose concentrations during the OGTT and a hyperglycemic clamp with arginine stimulation.</p> <p>The incretin effect was measured as 100*(AUC-SR<sub>OGTT </sub>– AUC-SR<sub>iso-IVGTT</sub>)/AUC-SR<sub>OGTT </sub>[AUC-SR=AUC of C-peptide secretion rate]. Participants were grouped into tertiles according to the percentage incretin effect (High-, Moderate- and Low-incretin effect) to describe their metabolic phenotype.</p> <p><b>Results </b>The presence of T risk allele for <i>TCF7L2</i> was associated with a markedly reduced </p> <p>incretin effect compared to the wild type genotype(0.3[-7.2,14] vs 37.8[12.5-52.4], p<0.002) When the cohort was stratified by incretin effect, the High-, Moderate- and Low-incretin groups did not differ with respect to anthropometric features, while the Low-incretin group exhibited higher 1-h glucose (p=0.015), a reduced disposition index, insulin sensitivity and insulin clearance, compared with the High-incretin group. Gastrointestinal induced glucose disposal (GIGD) was reduced in the Low-incretin group (p=0.001). The three groups did not differ with respect to intravenous glucose-induced insulin secretion and arginine response during the hyperglycemic clamp. </p> <p><b>Conclusion </b>A<b> </b> reduced incretin effect and its association with the <i>TCF7L2</i> variant rs7903146 identify an early metabolic phenotype in obese non-diabetic youths, featured by a higher plasma glucose peak at 1hr, lower insulin secretion, sensitivity and clearance, and gastrointestinal glucose disposal. </p>

scholarly journals Obstructive Sleep Apnea, Glucose Tolerance, and β-Cell Function in Adults With Prediabetes or Untreated Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

2021 ◽  
Author(s):  
Babak Mokhlesi ◽  
Ashley H. Tjaden ◽  
Karla A. Temple ◽  
Sharon L. Edelstein ◽  
Susan Sam ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Obstructive Sleep Apnea ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Sleep Duration ◽  
Beta Cell Function ◽  
Cell Function ◽  
Cell Responses ◽  
Obstructive Sleep

<b>Objective:</b> Obstructive sleep apnea (OSA) is associated with insulin resistance and has been described as a risk factor for type 2 diabetes. Whether OSA adversely impacts pancreatic islet beta-cell function remains unclear. We aimed to investigate the association of OSA and short sleep duration with beta-cell function in overweight/obese adults with prediabetes or recently-diagnosed, treatment-naïve type 2 diabetes. <p><b>Research Design and Methods:</b> 221 adults (57.5% men, age 54.5±8.7 years, BMI 35.1±5.5 kg/m<sup>2</sup>) completed one week of wrist actigraphy and one night of polysomnography before undergoing a 3-h oral glucose tolerance test (OGTT) and a two-step hyperglycemic clamp. Associations of measures of OSA and actigraphy-derived sleep duration with HbA1c, OGTT-derived and clamp-derived outcomes were evaluated with adjusted regression models.</p> <p><b>Results:</b> Mean±SD objective sleep duration by actigraphy was 6.6±1.0 hours/night. OSA defined as an apnea-hypopnea index (AHI) ≥5 events per hour was present in 89% of the participants; 20% mild, 28% moderate and 41% severe. Higher AHI was associated with higher HbA1c (p =0.007). However, OSA severity, measured by either AHI as a continuous variable or by categories of OSA severity, and sleep duration (continuous or <6 h vs. ≥6 h) were not associated with fasting glucose, 2-h glucose, insulin sensitivity or beta-cell responses.</p> <p><b>Conclusion:</b> In this baseline cross-sectional analysis of the RISE clinical trial of adults with prediabetes or recently-diagnosed, untreated type 2 diabetes, the prevalence of OSA was high. Although some measures of OSA severity were associated with HbA1c, OSA severity and sleep duration were not associated with measures of insulin sensitivity or beta-cell responses.</p>

scholarly journals Obstructive Sleep Apnea, Glucose Tolerance, and β-Cell Function in Adults With Prediabetes or Untreated Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

2021 ◽  
Author(s):  
Babak Mokhlesi ◽  
Ashley H. Tjaden ◽  
Karla A. Temple ◽  
Sharon L. Edelstein ◽  
Susan Sam ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Obstructive Sleep Apnea ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Sleep Duration ◽  
Beta Cell Function ◽  
Cell Function ◽  
Cell Responses ◽  
Obstructive Sleep

<b>Objective:</b> Obstructive sleep apnea (OSA) is associated with insulin resistance and has been described as a risk factor for type 2 diabetes. Whether OSA adversely impacts pancreatic islet beta-cell function remains unclear. We aimed to investigate the association of OSA and short sleep duration with beta-cell function in overweight/obese adults with prediabetes or recently-diagnosed, treatment-naïve type 2 diabetes. <p><b>Research Design and Methods:</b> 221 adults (57.5% men, age 54.5±8.7 years, BMI 35.1±5.5 kg/m<sup>2</sup>) completed one week of wrist actigraphy and one night of polysomnography before undergoing a 3-h oral glucose tolerance test (OGTT) and a two-step hyperglycemic clamp. Associations of measures of OSA and actigraphy-derived sleep duration with HbA1c, OGTT-derived and clamp-derived outcomes were evaluated with adjusted regression models.</p> <p><b>Results:</b> Mean±SD objective sleep duration by actigraphy was 6.6±1.0 hours/night. OSA defined as an apnea-hypopnea index (AHI) ≥5 events per hour was present in 89% of the participants; 20% mild, 28% moderate and 41% severe. Higher AHI was associated with higher HbA1c (p =0.007). However, OSA severity, measured by either AHI as a continuous variable or by categories of OSA severity, and sleep duration (continuous or <6 h vs. ≥6 h) were not associated with fasting glucose, 2-h glucose, insulin sensitivity or beta-cell responses.</p> <p><b>Conclusion:</b> In this baseline cross-sectional analysis of the RISE clinical trial of adults with prediabetes or recently-diagnosed, untreated type 2 diabetes, the prevalence of OSA was high. Although some measures of OSA severity were associated with HbA1c, OSA severity and sleep duration were not associated with measures of insulin sensitivity or beta-cell responses.</p>

Sign in / Sign up

Export Citation Format

Share Document