Excessive Purine Degradation druing Semi-ischemic Forearm Test in Patients with Diabetes Mellitus

Abstract

Objective The aim of this study was to investigate whether or not the purine degradation in the skeletal muscle during forearm exercise is augmentedin patients with diabetes mellitus (DM).Methods Weused the semi-ischemic forearm test to examine the release of lactate (ALAC), ammonia (AAmm) and hypoxanthine (AHX) before exercise, 0, 4, 10, and 60 minutes after exercise in eleven diabetic patients and seven normal controls. ResultsThe sum of the increased HX (DM vs Controls: 26.1±21.2 vs 7.8±5.9 umol//, p<0.05) was greater in diabetic patients. Whenpatients were divided into the excessive response group (n=7) and normal response group (n=4), the maximumincrements in AHXand A Amm in the excessive response group (16.8±3.2 umol// and 122±60 umol//) were greater (p<0.05) than those in the control group (3.6± 3.0 umol// and 32±34 umol//) and the normal response group (2.9±2.9 umol// and 27.4±12.7 umol//). ALACboth in the excessive response group (5.4±1.5 mmol//) and the normal response group (3.6±1.0 mmol//) were higher (p<0.05) than that of the control group (1.7±0.5 mmol//). The prevalence of diabetic retinopathy was higher in the excessive response group than in the normal response group (75% vs. 25%). Conclusion These data suggest that patients with DM, especially with microangiopathy have augmented purine degradation during the semi-ischemic forearm test. Factors responsible for the augmented purine degradation in these patients remain to be determined. (Internal Medicine 42: 788-792, 2003)

Newborn Meconium and Urinary Metabolome Response to Maternal Gestational Diabetes Mellitus: A Preliminary Case–Control Study

“…Three purine alkaloid metabolites (i.e., methyl­adenosine, methyl­guanosine, and uric acid) were tentatively identified, indicating dysfunction of the purine metabolism in GDM. Augmented purine degradation has been found in diabetes patients . The clinical significance of six related purine metabolites (adenosine, adenine, inosine, xanthine, hypo­xanthine, and uric acid) was assessed in diabetes patients’ plasma, and the results showed that levels of adenosine, inosine, uric acid, and xanthine may be useful for monitoring the progression of diabetes .…”

“…Augmented purine degradation has been found in diabetes patients. 40 The clinical significance of six related purine metabolites (adenosine, adenine, inosine, xanthine, hypoxanthine, and uric acid) was assessed in diabetes patients' plasma, and the results showed that levels of adenosine, inosine, uric acid, and xanthine may be useful for monitoring the progression of diabetes. 41 Uric acid is the final oxidation product of purine metabolism, and its level is lower in GDM cases relative to controls in this meconium metabolomics study.…”

Investigating correlations in the altered metabolic profiles of obese and diabetic subjects in a South Indian Asian population using an NMR-based metabolomic approach

“…Previously, semi-ischemic forearm test in T2DM subjects has revealed augmented purine metabolism, especially hypoxanthine degradation and associated increase in serum uric acid levels. 46 This might be an adaptive mechanism to support cellular energy in the absence of adequate glucose oxidation.…”

The supportive effect of supplementation with α-keto acids on physical training in type 2 diabetes mellitus

“…Although the mechanisms responsible for fatigue and exercise intolerance are not fully understood, a relationship between exercise-induced hyperammonemia and fatigue has been elucidated previously. 10 It has been shown that ammonia metabolism in diabetics was impaired compared with the non-diabetic controls. 7,8 Along with the increase in blood ammonia concentrations an increase in inosine-5′-monophosphate (IMP) and the ratio of IMP to AMP (adenosine monophosphate) was observed, indicating a deamination process from AMP to IMP under high energy turnover.…”

“…9 Excessive purine degradation along with a higher blood ammonia level was observed in diabetic subjects, in comparison with nondiabetic controls. 10 It has been shown that ammonia metabolism in diabetics was impaired compared with the non-diabetic controls. 11 Previous studies have shown that protein breakdown leading to an increase in the blood concentration of amino acids is augmented in T2D.…”