Intravenous glucose tolerance and pancreatic islet beta-cell function in patients with multiple sclerosis during 2-yr treatment with cyclosporin

Diabetes ◽  
1989 ◽  
Vol 38 (1) ◽  
pp. 58-64 ◽  
Author(s):  
R. P. Robertson ◽  
G. Franklin ◽  
L. Nelson
2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
M. Ladwa ◽  
O. Hakim ◽  
S. A. Amiel ◽  
L. M. Goff

Background. Understanding ethnic differences in beta cell function has important implications for preventative and therapeutic strategies in populations at high risk of type 2 diabetes (T2D). The existing literature, largely drawn from work in children and adolescents, suggests that beta cell function in black African (BA) populations is upregulated when compared to white Europeans (WE). Methods. A systematic literature search was undertaken in June 2018 to identify comparative studies of beta cell function between adults (>age 18 years) of indigenous/diasporic BA and WE ethnicity. All categories of glucose tolerance and all methodologies of assessing beta cell function in vivo were included. Results. 41 studies were identified for inclusion into a qualitative synthesis. The majority were studies in African American populations (n=30) with normal glucose tolerance (NGT)/nondiabetes (n=25), using intravenous glucose stimulation techniques (n=27). There were fewer studies in populations defined as only impaired fasting glucose/impaired glucose tolerance (IFG/IGT) (n=3) or only T2D (n=3). Although BA broadly exhibited greater peripheral insulin responses than WE, the relatively small number of studies which measured C-peptide to differentiate between beta cell insulin secretion and hepatic insulin extraction (n=14) had highly variable findings. In exclusively IGT or T2D cohorts, beta cell insulin secretion was found to be lower in BA compared to WE. Conclusions. There is inconsistent evidence for upregulated beta cell function in BA adults, and they may in fact exhibit greater deficits in insulin secretory function as glucose intolerance develops.


1996 ◽  
Vol 270 (4) ◽  
pp. E572-E579 ◽  
Author(s):  
M. M. Byrne ◽  
J. Sturis ◽  
R. J. Sobel ◽  
K. S. Polonsky

Studies were performed in subjects with no known family history of diabetes, normoglycemic subjects who have first-degree relatives with non-insulin-dependent diabetes mellitus (NIDDM), and subjects with nondiagnostic oral glucose tolerance tests (NDX) or impaired glucose tolerance (IGT). Insulin sensitivity index (SI) was similar in all four groups. However, a number of defects in insulin secretion were seen in the NDX and IGT groups, including reduced first-phase insulin secretory responses in intravenous glucose in relation to the degree of insulin resistance, and reduced normalized spectral power of insulin secretion during oscillatory glucose infusion. The latter finding demonstrates a decreased ability of the beta-cell to detect and respond to the successive increases and decreases in glucose and therefore to be entrained by the exogenous glucose infusion. The ability of a low-dose glucose infusion to prime the insulin secretory response to a subsequent glucose stimulus was normal in subjects with IGT but reduced or absent in subjects with overt NIDDM. These studies demonstrate that a number of alterations in beta-cell function are detectable in nondiabetic first-degree relatives of subjects with NIDDM with mild elevations in the 2-h postchallenge glucose level, and these abnormalities antedate the onset of overt hyperglycemia and clinical diabetes.


1960 ◽  
Vol XXXIII (II) ◽  
pp. 157-167
Author(s):  
T. Rodari ◽  
G. Specchia

ABSTRACT The double intravenous glucose tolerance test does not modify the assimilation coefficient in normal and thin diabetic subjects. On the contrary, in fat diabetic subjects the second coefficient of assimilation increases significantly, but not the first one. From these researches it is evident that the valuation of glucose assimilation by double venous hyperglycaemic test indicates the functional behaviour of the pancreas in different diabetic states. The interpretation of this behaviour of pancreatic islet response to the double venous hyperglycaemic test is discussed.


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