scholarly journals Proinsulin-to-C-peptide ratio versus proinsulin-to-insulin ratio in the prediction of incident diabetes: the Insulin Resistance Atherosclerosis Study (IRAS)

Diabetologia ◽  
2011 ◽  
Vol 54 (12) ◽  
pp. 3047-3054 ◽  
Author(s):  
R. C. Loopstra-Masters ◽  
S. M. Haffner ◽  
C. Lorenzo ◽  
L. E. Wagenknecht ◽  
A. J. Hanley
2011 ◽  
Vol 10 (8) ◽  
pp. 921-927 ◽  
Author(s):  
Shaheena Banu ◽  
Nasimudeen R. Jabir ◽  
C. N. Manjunath ◽  
Shazi Shakil ◽  
Mohammad A. Kamal

2021 ◽  
Vol 2 (1) ◽  
pp. 49-56
Author(s):  
Valeria Cademartori ◽  
Fabio Massarino ◽  
Emanuele L. Parodi ◽  
Ernesto Paoletti ◽  
Rodolfo Russo ◽  
...  

The use of tacrolimus (Tac) may be involved in the development of new-onset diabetes after transplantation (NODAT) in a dose-related manner. This study aimed to evaluate the effects of a standard twice-daily formulation of Tac (TacBID) vs. the once-daily slow-release formulation (TacOD) on the basal insulin resistance indexes (Homa and McAuley), and related metabolic parameters, in a cohort of kidney transplant patients. We retrospectively evaluated 20 stable renal transplant recipients who were switched from TacBID to TacOD. Blood levels of Tac were analyzed at one-month intervals from 6 months before to 8 months after conversion. Moreover, Homa and McAuley indexes, C-peptide, insulin, HbA1c, uric acid, triglycerides, low-density lipoprotein (LDL) and high-density lipoprotein (HDL)-cholesterol serum levels and their associations with Tac levels were evaluated. We observed a significant decrease in Tac exposure (8.5 ± 2 ng/mL, CV 0.23 vs. 6.1 ± 1.9 ng/mL, CV 0.31, TacBID vs. TacOD periods, p < 0.001) and no significant changes in Homa (1.42 ± 0.4 vs. 1.8 ± 0.7, p > 0.05) and McAuley indexes (7.12 ± 1 vs. 7.58 ± 1.4, p > 0.05). Similarly, blood levels of glucose, insulin, HbA1c, lipids, and uric acid were unchanged between the two periods, while C-peptide resulted significantly lower after conversion to TacOD. These data suggest that in kidney transplant recipients, reduced Tac exposure has no significant effects on basal insulin sensitivity indexes and metabolic parameters.


Diabetes Care ◽  
2004 ◽  
Vol 27 (3) ◽  
pp. 781-787 ◽  
Author(s):  
M. Rewers ◽  
D. Zaccaro ◽  
R. D'Agostino ◽  
S. Haffner ◽  
M. F. Saad ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Gorica G. Ristić ◽  
Vesna Subota ◽  
Dejana Stanisavljević ◽  
Danilo Vojvodić ◽  
Arsen D. Ristić ◽  
...  

Abstract Objective To explore glucose metabolism in rheumatoid arthritis (RA) and its association with insulin resistance (IR) risk factors and disease activity indicators, including matrix metalloproteinase-3 (MMP3). Methods This single-center study included 127 non-diabetic subjects: 90 RA patients and 37 matched controls. IR-related risk factors, disease activity (DAS28-ESR/CRP), concentrations of inflammation markers, MMP3, glucose, specific insulin, and C-peptide (a marker of β-cell secretion) were determined. Homeostasis Model Assessment was used to establish insulin resistance (HOMA2-IR) and sensitivity (HOMA2-%S). Associations of HOMA2 indices with IR-related risk factors, inflammation markers, and RA activity were tested using multiple regression analyses. Results RA patients had significantly increased HOMA2-IR index than controls. In the RA group, multivariate analysis revealed DAS28-ESR, DAS28-CRP, tender joint counts, patient’s global assessment, and MMP3 level as significant positive predictors for HOMA2-IR (β = 0.206, P = 0.014; β = 0.192, P = 0.009; β = 0.121, P = 0.005; β = 0.148, P = 0.007; β = 0.075, P = 0.025, respectively), and reciprocal negative for HOMA2-%S index. According to the value of the coefficient of determination (R2), DAS28-ESR ≥ 5.1 has the largest proportion of variation in both HOMA2-IR indices. DAS28-ESR ≥ 5.1 and ESR were independent predictors for increased C-peptide concentration (β = 0.090, P = 0.022; β = 0.133, P = 0.022). Despite comparability regarding all IR-related risk factors, patients with DAS28-ESR ≥ 5.1 had higher HOMA2-IR than controls [1.7 (1.2–2.5) vs. 1.2 (0.8–1.4), P = 0.000]. There was no difference between patients with DAS28-ESR < 5.1 and controls [1.3 (0.9–1.9) vs. 1.2 (0.8–1.4), P = 0.375]. Conclusions RA activity is an independent risk factor for impaired glucose metabolism. DAS28-ESR ≥ 5.1 was the main contributor to this metabolic disturbance, followed by MMP3 concentration, outweighing the impact of classic IR-related risk factors.


2008 ◽  
Vol 294 (3) ◽  
pp. E568-E575 ◽  
Author(s):  
Johannes Erdmann ◽  
Bianca Kallabis ◽  
Ulrich Oppel ◽  
Oleg Sypchenko ◽  
Stefan Wagenpfeil ◽  
...  

Obesity is associated with insulin resistance and hyperinsulinemia, which is considered to be a core component in the pathophysiology of obesity-related comorbidities. As yet it is unknown whether insulin resistance and hyperinsulinemia already develop during weight gain within the normal range. In 10 healthy male subjects the effect of intentional weight gain by 2 BMI points was examined on insulin. C-peptide and glucose levels following a meal, 75 g of glucose, and a two-step hyperglycemic clamp increased plasma glucose by 1.38 and 2.75 mmol/l, respectively. Baseline insulin, C-peptide, and glucose concentrations were significantly higher after weight gain from 21.8 to 23.8 kg/m2 BMI within 41/2 mo. Calculations of insulin secretion and clearance indicate that reduced insulin clearance contributes more to post-weight gain basal hyperinsulinemia than insulin secretion. Following oral or intravenous stimulation insulin concentrations were significantly higher post-weight gain during all three test conditions, whereas C-peptide and glucose levels did not differ. Calculations of insulin secretion and clearance demonstrated that higher stimulated insulin concentrations are entirely due to clearance but not secretion. Despite significantly higher insulin levels, the rate of intravenous glucose required to maintain the defined elevation of glucose levels was either identical (1.38 mmol/l) or even significantly lower (2.75 mmol/l) following weight gain. The present study demonstrates for the first time that insulin resistance already develops during weight gain within the normal range of body weight. The associated basal and stimulated hyperinsulinemia is the result of differentiated changes of insulin secretion and clearance, respectively.


2020 ◽  
Vol 18 (5) ◽  
pp. 93-98
Author(s):  
L. B. NOVIKOVA ◽  
◽  
G. I. IZHBULDINA ◽  

Among the reasons that increase the risk of stroke, its severity and outcome, a special place is given to disorders of carbohydrate metabolism. However, to date, there is no consensus on the role of hyperglycemia in stroke, whether it is physiological or pathological. The purpose to study the effect of insulin resistance on the course and clinical outcome of ischemic stroke (IS) in the acute period. Material and methods. A total of 862 patients with IS (370 men, 492 women), mean age was 66,1 ± 10,8 years. The degree of neurological deficit (NIHSS scale) and clinical outcome were assessed. When admitted to hospital, the level of glycemia, insulin, and C-peptide in the fasting blood were found. Results. In 186 (21,6%) patients type 2 diabetes mellitus (DM) was diagnosed. In 27,8% of patients without DM and 76,3% of patients with DM hyperglycemia was detected. In patients without DM with hyperglycemia, compared with patients with normoglycemia, a higher representation of severe neurological deficit (by 14,7%), a lower frequency of noticeable positive dynamics (by 14,8%), and a higher mortality rate (by 11,5%) were found. In patients with DM, hyperglycemia was associated with a lower incidence of noticeable positive dynamics (by 27,7%). The development of IS is accompanied by an increase in the blood level of C-peptide more than twice. High values of the C-peptide/insulin ratio are associated with a higher frequency of severe neurological deficit in patients with DM (by 32,4%) and without DM (by 23,8%), and a decrease in the incidence of noticeable positive dynamics (by 23,5% and 20,9%, respectively). Conclusion. Development of IS is characterized by high representation of disorders of carbohydrate metabolism. The severity of glucose metabolism disorders is interrelated with the severity and clinical outcome of the disease.


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