Adiponectin and Leptin are Independently Associated with Insulin Sensitivity, but not with Insulin Secretion or Beta-cell Function in Overweight Hispanic Adolescents

2008 ◽  
Vol 40 (10) ◽  
pp. 708-712 ◽  
Author(s):  
C. Koebnick ◽  
C. Roberts ◽  
G. Shaibi ◽  
L. Kelly ◽  
C. Lane ◽  
...  
2004 ◽  
pp. 97-104 ◽  
Author(s):  
B Ahren ◽  
G Pacini

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.


2021 ◽  
Vol 9 (1) ◽  
pp. e002034
Author(s):  
Meera Ladwa ◽  
Oluwatoyosi Bello ◽  
Olah Hakim ◽  
Fariba Shojaee-Moradie ◽  
Maria Linda Boselli ◽  
...  

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.


1983 ◽  
Vol 104 (4_Suppl) ◽  
pp. S131-S135
Author(s):  
Leif Groop ◽  
Risto Pelkonen

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.


Diabetes ◽  
1996 ◽  
Vol 45 (11) ◽  
pp. 1572-1579 ◽  
Author(s):  
K. Berkowitz ◽  
R. Peters ◽  
S. L. Kjos ◽  
J. Goico ◽  
A. Marroquin ◽  
...  

Plants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 286
Author(s):  
Nicola Marrano ◽  
Rosaria Spagnuolo ◽  
Giuseppina Biondi ◽  
Angelo Cignarelli ◽  
Sebastio Perrini ◽  
...  

Extra virgin olive oil (EVOO) is a major component of the Mediterranean diet and is appreciated worldwide because of its nutritional benefits in metabolic diseases, including type 2 diabetes (T2D). EVOO contains significant amounts of secondary metabolites, such as phenolic compounds (PCs), that may positively influence the metabolic status. In this study, we investigated for the first time the effects of several PCs on beta-cell function and survival. To this aim, INS-1E cells were exposed to 10 μM of the main EVOO PCs for up to 24 h. Under these conditions, survival, insulin biosynthesis, glucose-stimulated insulin secretion (GSIS), and intracellular signaling activation (protein kinase B (AKT) and cAMP response element-binding protein (CREB)) were evaluated. Hydroxytyrosol, tyrosol, and apigenin augmented beta-cell proliferation and insulin biosynthesis, and apigenin and luteolin enhanced the GSIS. Conversely, vanillic acid and vanillin were pro-apoptotic for beta-cells, even if they increased the GSIS. In addition, oleuropein, p-coumaric, ferulic and sinapic acids significantly worsened the GSIS. Finally, a mixture of hydroxytyrosol, tyrosol, and apigenin promoted the GSIS in human pancreatic islets. Apigenin was the most effective compound and was also able to activate beneficial intracellular signaling. In conclusion, this study shows that hydroxytyrosol, tyrosol, and apigenin foster beta-cells’ health, suggesting that EVOO or supplements enriched with these compounds may improve insulin secretion and promote glycemic control in T2D patients.


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