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.

Metabolomic Characteristics of Fatty Pancreas

2019 ◽  
Vol 128 (12) ◽  
pp. 804-810 ◽  
Author(s):  
Benjamin Assad Jaghutriz ◽  
Róbert Wagner ◽  
Martin Heni ◽  
Rainer Lehmann ◽  
Jürgen Machann ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Visceral Fat ◽  
Beta Cell Function ◽  
Cell Function ◽  
Fat Content ◽  
Pancreatic Fat ◽  
Total Body ◽  
Pancreatic Steatosis ◽  
Pancreatic Fat Content

Abstract Objective Pancreatic steatosis is associated with impaired beta cell function in patients with prediabetes. The pathomechanisms underlying this association still remain to be elucidated. Recent data show that adipocytes are situated within the pancreatic parenchyma and therefore give raise to hypothesize that pancreatic fat together with known and unknown metabolites such as hepatokines affect insulin secretion. Applying a targeted metabolomic approach we investigated possible circulating markers of pancreatic fat in order to better understand its role in the pathophysiology of impaired beta cell function. Methods We included 361 Caucasians, at increased risk of type 2 diabetes, from the Tübingen Family Study. All participants underwent a frequently sampled oral glucose tolerance test to assess insulin secretion and a magnetic resonance imaging to quantify pancreatic fat content, total body fat and visceral fat. Among the 152 subjects with prediabetes (IFG and/or IGT), two groups each with 20 individuals, having the lowest and highest pancreatic fat content were selected. The groups were matched for sex, age, BMI, total fat content, visceral fat content, liver fat content and insulin sensitivity. Metabolites were analyzed using the AbsoluteIDQ® p400 HR Kit by Biocrates. Results Pancreatic fat content of all 152 subjects with prediabetes was negatively associated with insulin secretion represented by AUCC-peptide 0–120/AUCGlucose 0–120 (p=0.04; β=− 3.24). Furthermore, pancreatic fat content was positively associated with BMI, total body and visceral fat (all p<0.005). Levels of aminoacids, biogenic amines and monosaccharides were similar between the groups with high/low pancreatic fat content (p>0.90). Also, levels of polar lipids such as lysophosphatidylcholines, phosphatidylcholines, sphingomyelins and ceramides did not differ significantly between the groups (p>0.90). Investigating the levels of neutral lipids such as aclycarnitines, diglycerides, triglycerides and cholesteryl esters also revealed no differences between the groups (p>0.90). Conclusion The amount of pancreatic fat is not associated with the metabolomic pattern in individuals with prediabetes. This might be due to the relatively low pancreatic fat content compared to the total amount of fat stored in other depots. The impact of pancreatic steatosis on insulin secretion might be mediated by paracrine effects which cannot be detected in the circulation.

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 insulin sensitivity and beta-cell function among Asian men

2015 ◽  
Vol 5 (7) ◽  
pp. e173-e173 ◽  
Author(s):  
V M H Tan ◽  
Y S Lee ◽  
K Venkataraman ◽  
E Y H Khoo ◽  
E S Tai ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Beta Cell ◽  
Ethnic Differences ◽  
Beta Cell Function ◽  
Cell Function ◽  
Asian Men

scholarly journals Pancreatic Steatosis Associates With Impaired Insulin Secretion in Genetically Predisposed Individuals

2020 ◽  
Vol 105 (11) ◽  
Author(s):  
Róbert Wagner ◽  
Benjamin Assad Jaghutriz ◽  
Felicia Gerst ◽  
Morgana Barroso Oquendo ◽  
Jürgen Machann ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Genetic Risk ◽  
Beta Cell Function ◽  
Cell Function ◽  
Polygenic Score ◽  
High Genetic Risk ◽  
Pancreatic Fat ◽  
Genome Wide ◽  
Pancreatic Steatosis

Abstract Context Pancreatic steatosis leading to beta-cell failure might be involved in type 2 diabetes (T2D) pathogenesis. Objective We hypothesized that the genetic background modulates the effect of pancreatic fat on beta-cell function and investigated genotype × pancreatic fat interactions on insulin secretion. Design Two observational studies. Setting University hospital. Patients or participants A total of 360 nondiabetic individuals with elevated risk for T2D (Tuebingen Family Study [TUEF]), and 64 patients undergoing pancreatectomy (Pancreas Biobank [PB], HbA1c &lt;9%, no insulin therapy). Main Outcome Measures Insulin secretion calculated from 5-point oral glucose tolerance test (TUEF) and fasting blood collection before surgery (PB). A genome-wide polygenic score for T2D was computed from 484,788 genotyped variants. The interaction of magnetic resonance imaging-measured and histologically quantified pancreatic fat with the polygenic score was investigated. Partitioned risk scores using genome-wide significant variants were also computed to gain insight into potential mechanisms. Results Pancreatic steatosis interacted with genome-wide polygenic score on insulin secretion (P = 0.003), which was similar in the replication cohort with histological measurements (P = 0.03). There was a negative association between pancreatic fat and insulin secretion in participants with high genetic risk, whereas individuals with low genetic risk showed a positive correlation between pancreatic fat and insulin secretion. Consistent interactions were found with insulin resistance-specific and a liver/lipid-specific polygenic scores. Conclusions The associations suggest that pancreatic steatosis only impairs beta-cell function in subjects at high genetic risk for diabetes. Genetically determined insulin resistance specifically renders pancreatic fat deleterious for insulin secretion.

Treatment failures: A common problem in the management of patients with type II diabetes

1983 ◽  
Vol 104 (4_Suppl) ◽  
pp. S131-S135
Author(s):  
Leif Groop ◽  
Risto Pelkonen
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Special Interest ◽  
Type Ii Diabetes ◽  
Beta Cell Function ◽  
Cell Function ◽  
Type Ii ◽  
Secondary Failure ◽  
Secondary Drug Failure

ABSTRACT. Secondary failure is a common problem in the treatment of patients with type II diabetes. The underlying mechanisms are reviewed, and special interest is focused on the assessment of insulin secretion and insulin sensitivity. Impaired beta-cell function seems to be the major cause of secondary drug failure in patients with normal weight, whereas insulin resistance is of greater importance in obese patients. The importance of Cpeptide determinations to detect patients needing insulin is emphasized. The concept of progressive deterioration of beta-cell function with time in type II diabetes is challenged. Different treatment modalities for the management of patients with secondary drug failure are discussed and special interest is focused on the combination of insulin and sulfonylureas in the management of secondary failure patients with slightly impaired insulin secretion. Key words: secondary drug failure, type II diabetes, Cpeptide, insulin sensitivity, oral antidiabetic drugs, insulin therapy.

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