acid-phosphatase and Diabetes-Mellitus--Type-1

Bone mineral density (BMD) at the lumbar spine, quantified by dual energy X-ray absorptiometry, and biochemical bone remodeling markers (serum alkaline phosphatase, osteocalcin, tartrate-resistant acid phosphatase and urinary hydroxyproline) have been studied in 94 patients with diabetes mellitus aged 18-62 years. BMD was normal (1.13 +/- 0.02 g/cm2 in patients vs. 1.16 +/- 0.12 g/cm2 in controls), although it was found to be negatively correlated with HbA1, microalbuminuria, age and the duration of the disease. Serum alkaline phosphatase (188 +/- 75 I.U./l vs. 168 +/- 42 I.U./1; P < 0.03), serum tartrate-resistant acid phosphatase (14.3 +/- 4.3 I.U./l vs. 11.7 +/- 3.7 I.U./l; P < 0.0001) and urinary hydroxyproline (0.018 +/- 0.016 mmol/mmol creatinine vs. 0.011 +/- 0.008 mmol/mmol creatinine; P < 0.001) were higher in diabetics than in controls. Serum osteocalcin was lower (2.5 +/- 1.3 ng/ml vs. 3.4 +/- 1.2 ng/ml; P < 0.0001). No relationship was found between bone remodeling markers and BMD. It is concluded that lumbar BMD is normal in type 1 diabetic patients, although the degree of metabolic control, age and duration of the disease may affect it. In the light of the biochemical markers, bone remodeling may be disturbed in diabetes, but such disturbance seems to be unimportant regarding BMD.

Topics: Acid Phosphatase; Adolescent; Adult; Alkaline Phosphatase; Biomarkers; Bone and Bones; Bone Density; Bone Remodeling; Creatinine; Densitometry; Diabetes Mellitus, Type 1; Female; Humans; Hydroxyproline; Male; Middle Aged; Minerals; Osteocalcin

There are contradictory results about the effect of angiotensin-converting enzyme inhibitors (ACEIs) on bone. This study was performed to address the skeletal renin-angiotensin system (RAS) activity and the effects of the ACEI, captopril, on the bone of streptozotocin-induced type 1 diabetic mice. Histochemical assessment on bone paraffin sections was conducted by Safranin O staining and tartrate-resistant acid phosphatase staining. Micro-computed tomography was performed to analyze bone biological parameters. Gene and protein expression were determined by real-time polymerase chain reaction and immunoblotting, respectively. Type 1 diabetic mice displayed osteopenia phenotype and captopril treatment showed no osteoprotective effects in diabetic mice as shown by the reduction of bone mineral density, trabecular thickness and bone volume/total volume. The mRNA expression of ACE and renin receptor, and the protein expression of renin and angiotensin II were markedly up-regulated in the bone of vehicle-treated diabetic mice compared to those of non-diabetic mice, and these molecular changes of skeletal RAS components were effectively inhibited by treatment with captopril. However, treatment with captopril significantly elevated serum tartrate-resistant acid phosphatase 5b levels, reduced the ratio of osteoprotegerin/receptor activator of nuclear factor-κB ligand expression, increased carbonic anhydrase II mRNA expression and the number of matured osteoclasts and decreased transforming growth factor-β and osteocalcin mRNA expression in the tibia compared to those of diabetic mice. The present study demonstrated that the use of the ACEI, captopril, has no beneficial effect on the skeletal biological properties of diabetic mice. However, this could be attributed, at least partially, to its suppression of osteogenesis and stimulation of osteoclastogenesis, even though it could effectively inhibit high activity of local RAS in the bone of diabetic mice.

Topics: Acid Phosphatase; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Bone and Bones; Bone Density; Bone Diseases, Metabolic; Captopril; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Isoenzymes; Male; Mice; Mice, Inbred DBA; NF-kappa B; Osteocalcin; Osteoclasts; Random Allocation; Renin; Renin-Angiotensin System; RNA, Messenger; Streptozocin; Tartrate-Resistant Acid Phosphatase; Tibia; Transforming Growth Factor beta; Up-Regulation

Type 1 diabetic osteoporosis results from impaired osteoblast activity and death. Therefore, anti-resorptive treatments may not effectively treat bone loss in this patient population. Intermittent parathyroid hormone (PTH) treatment stimulates bone remodeling and increases bone density in healthy subjects. However, PTH effects may be limited in patients with diseases that interfere with its signaling. Here, we examined the ability of 8 and 40 µg/kg intermittent PTH to counteract diabetic bone loss. PTH treatment reduced fat pad mass and blood glucose levels in non-diabetic PTH-treated mice, consistent with PTH-affecting glucose homeostasis. However, PTH treatment did not significantly affect general body parameters, including the blood glucose levels, of type 1 diabetic mice. We found that the high dose of PTH significantly increased tibial trabecular bone density parameters in control and diabetic mice, and the lower dose elevated trabecular bone parameters in diabetic mice. The increased bone density was due to increased mineral apposition and osteoblast surface, all of which are defective in type 1 diabetes. PTH treatment suppressed osteoblast apoptosis in diabetic bone, which could further contribute to the bone-enhancing effects. In addition, PTH treatment (40 µg/kg) reversed preexisting bone loss from diabetes. We conclude that intermittent PTH may increase type 1 diabetic trabecular bone volume through its anabolic effects on osteoblasts.

Topics: Acid Phosphatase; Animals; Bone Density; Bone Remodeling; Bone Resorption; Cell Survival; Diabetes Complications; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Humans; Isoenzymes; Male; Mice; Mice, Inbred BALB C; Osteoblasts; Osteogenesis; Osteoporosis; Parathyroid Hormone; RNA, Messenger; Tartrate-Resistant Acid Phosphatase

Diabetes is known to impair wound healing and deteriorate the periodontal condition. There is limited information about the patterns and events associated with periodontal wound repair. In this study, we evaluate the dynamics of periodontal wound repair using micro-computed tomography (microCT) and immunohistochemistry.. Thirty-six male rats were used, and diabetes was induced by streptozotocin. The maxillary first molars were extracted, and a tooth-associated osseous defect was created in the extraction area. Animals were sacrificed after 7, 14, and 21 days. Volumetry and distribution of bone trabeculae were evaluated by microCT imaging. The patterns of healing and collagen alignment were evaluated by histology. Advanced glycation end-product (AGE) deposition and expression of the receptor for AGEs (RAGE), tartrate-resistant acid phosphatase, and proliferating cell nuclear antigen were evaluated by histochemical and immunohistochemical staining.. Diabetic animals demonstrated a significantly reduced bone volume and trabecular number as well as thinner trabeculae and more trabecular separation in osseous defects. The early stage was characterized by significantly reduced cellular proliferation and prolonged active inflammation without evident bone resorption, whereas delayed recovery of collagen realignment, matrix deposition, and bone turnover was noted in later stages. Although AGEs and RAGE were present during healing in diabetes and controls, a stronger and more persistent level of expression was observed in the group with diabetes. Diabetes significantly delayed osseous defect healing by augmenting inflammation, impairing proliferation, and delaying bone resorption. The AGE-RAGE axis can be activated under metabolic disturbance and inflammation.

Topics: Acid Phosphatase; Alveolar Bone Loss; Animals; Bone Remodeling; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Fibrillar Collagens; Glycation End Products, Advanced; Immunohistochemistry; Isoenzymes; Male; Periodontitis; Proliferating Cell Nuclear Antigen; Rats; Rats, Sprague-Dawley; Receptor for Advanced Glycation End Products; Receptors, Immunologic; Tartrate-Resistant Acid Phosphatase; Wound Healing; X-Ray Microtomography

The present study was taken up to assess the role of subchronic exposure to an environmentally relevant dosage of cadmium in type l diabetes. Female rats of the Wistar strain were treated with cadmium (5.12 mg/kg body weight) for 45 days. On day 46, rats were made diabetic by alloxan. After 7 days, diabetes (i.e., animals with serum glucose greater than 300 mg/dL) in the alloxanized animals was confirmed and further experiments were conducted for 15 days. Cadmium pretreatment showed disturbed glucose homeostasis with attendant changes in carbohydrate metabolism, coupled with decrease in food and water intake. Disturbance in carbohydrate metabolism was indicated by altered tissue metabolite load, as marked by a decrease in protein and glycogen contents and increased cholesterol store. Poor glucose clearance subsequent to a glucose challenge under the glucose tolerance test was observed in these animals (0.48/min in control vs. 0.13/min in Cd animals). There was a significantly lower glucose elevation rate in the insulin response test subsequent to an insulin-induced decrease in glucose level in Cd-exposed animals. Elevated oxidative stress was marked by increased lipid peroxidation, decreased antioxidant (both nonenzymatic and enzymatic) levels, and serum markers of hepatic and renal damage. Decreased corticosterone levels, together with increased E2 and reduced P4 levels, were some of the hallmark changes in the serum hormone profile of Cd-exposed animals. Overall, the present results are novel and interesting to open more investigations on animal models of type 1 diabetes with a history of previous Cd exposure.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Blood Glucose; Cadmium; Cadmium Poisoning; Cholesterol; Corticosterone; Diabetes Mellitus, Type 1; Drinking; Eating; Estradiol; Female; Glucose Tolerance Test; Insulin; Kidney; Liver; Progesterone; Rats; Rats, Wistar; Triglycerides

Orthodontic tooth movement is achieved by the remodeling of alveolar bone in response to mechanical loading. Type 1 diabetes results in bone remodeling, suggesting that this disease might affect orthodontic tooth movement. The present study investigated the effects of the diabetic state on orthodontic tooth movement. An orthodontic appliance was placed in normoglycemic (NG), streptozotocin-induced diabetes (DB), and insulin-treated DB (IT) C57BL6/J mice. Histomorphometric analysis and quantitative PCR of periodontium were performed. The DB mice exhibited greater orthodontic tooth movement and had a higher number of tartrate-resistant acid phosphate (TRAP) -positive osteoclasts than NG mice. This was associated with increased expression of factors involved in osteoclast activity and recruitment (Rankl, Csf1, Ccl2, Ccl5, and Tnfa) in DB mice. The expression of osteoblastic markers (Runx2, Ocn, Col1, and Alp) was decreased in DB mice. Reversal of the diabetic state by insulin treatment resulted in morphological findings similar to those of NG mice. These results suggest that the diabetic state up-regulates osteoclast migration and activity and down-regulates osteoblast differentiation, resulting in greater orthodontic tooth movement.

Topics: Acid Phosphatase; Alveolar Process; Animals; Bone Remodeling; Cell Differentiation; Cell Movement; Chemokines; Cytokines; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Disease Models, Animal; Insulin; Isoenzymes; Male; Mice; Mice, Inbred C57BL; Osteoblasts; Osteoclasts; Periodontal Ligament; Tartrate-Resistant Acid Phosphatase; Tooth Movement Techniques

Insulin-dependent diabetes mellitus (IDDM) is known to be associated with an increased risk of osteopenia. However, the cellular and molecular mechanisms for IDDM-induced alterations of the bone are not well understood. The effects of IDDM on bone metabolism were investigated using rats rendered diabetic by an injection of streptozotocin (STZ). After 4 weeks, the diabetic rats exhibited bone loss, low levels of osteocalcin, insulin-like growth factor-I (IGF-I) and bone alkaline phosphatase (ALP) activity with normal levels of bone tartrate-resistant acid phosphatase (TRAP) and cathepsin K activity, and urinary excretion of deoxypyridinoline (Dpd). Histological analysis showed a decrease in the number of osteoblasts with a normal number of osteoclasts in the metaphysis of the proximal tibia. The decreased expression of ALP, osteoclacin and collagen mRNA was associated with a decrease in the expression of runt-related transcription factor 2 (Runx2), Osterix and distal-less homeobox 5 (Dlx5) and an unaltered expression of bone morphogenic protein-2 (BMP2). The protein levels of Runx2, phosphorylated glycogen synthase kinase 3β (GSK3β), active β-catenin and β-catenin decreased. The activation of Akt was inhibited. The mRNA and protein levels of sclerosteosis (Sost) and Dickkopf 1 (Dkk1), inhibitors of Wnt signaling, increased. The mRNA expression of IGF-I and the IGF-I receptor (IGF-IR) was suppressed. These changes observed in the bone of diabetic rats were reversed by treatment with insulin, but not by normalization of the circulating IGF-I levels by treatment with IGF-I. These results suggest that insulin-deficiency in IDDM decreases osteoblastogenesis associated with inhibition of Wnt signaling through the increased expression of Sost and Dkk1 and the inhibition of Akt activation.

Topics: Acid Phosphatase; Alkaline Phosphatase; Amino Acids; Animals; beta Catenin; Bone Morphogenetic Protein 2; Bone Morphogenetic Proteins; Cathepsin K; Core Binding Factor Alpha 1 Subunit; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Female; Genetic Markers; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Homeodomain Proteins; Insulin-Like Growth Factor I; Intercellular Signaling Peptides and Proteins; Isoenzymes; Osteoblasts; Osteocalcin; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Signal Transduction; Tartrate-Resistant Acid Phosphatase; Transcription Factors; Wnt Proteins

Ability to respond to environmental changes and secretion of hydrolases are considered to be important for Candida virulence. In this study we determined and compared the activities of 19 different hydrolases of the fungal strains isolated from diabetic and non-diabetic pregnant women. We also looked for the presence of a relationship between hydrolase activities and glycemic control, and, furthermore, evaluated the influence of gestational age on the activity of hydrolases. Mycological examinations were performed for 119 diabetic pregnant women: 47 with diabetes mellitus type I (DM), 72 with gestational diabetes (GDM), and for 132 healthy women (CON). Samples were collected from the vagina, rectum and oral cavity and cultured on Sabouraud media. The fungal hydrolase activities were evaluated using the API ZYM test (bioMerieux). For the 19 different fungal hydrolases tested, 13 activities were present in the isolated fungal strains. The activity of alkaline phosphatase (ALP) in vaginal strains (p=0.028) and acid phosphatase (ACP) in strains from the vagina (p=0.006) and rectum (p=0.049) was significantly lower in DM than in GDM and CON women. In conclusion, we describe for the first time that fungi isolated from pregnant diabetic women have lower activity of both phosphatases compared to fungi isolated from healthy women. Furthermore, similar differences of mean ALP and ACP activities were observed in the course of pregnancy in strains from the vagina and rectum of DM and CON women. However, strains from DM had lower activity at each stage of pregnancy. The highest activity of ALP and ACP was detected at the beginning, then declined, and had the lowest values between the 24(th) and 33(rd) week of gestation. After that period the activity of both phosphatases increased.

Topics: Acid Phosphatase; Alkaline Phosphatase; Blood Glucose; Candida; Candida albicans; Candidiasis; Case-Control Studies; Diabetes Mellitus, Type 1; Diabetes, Gestational; Female; Fungi; Humans; Mycoses; Pregnancy; Pregnancy Complications, Infectious; Pregnancy in Diabetics; Rectum; Vagina; Virulence

The ability of insulin to influence activities of various protein kinases and protein phosphatases, that are thought to mediate insulin action, are limited in patients with insulin resistance. Because numerous responses to insulin are affected, we undertook studies to determine whether protein tyrosine phosphatases (PTPs) activities are altered in patients with diabetes syndrome. In order to evaluate abnormal PTP activities, we done a comparative study using erythrocytes from normal and diabetic patients. We determined the activity of the cytosolic acid PTP in basal and insulin-dependent states. Mean basal PTP activities, were found to be significantly higher in diabetics than in normal subjects (type 1 diabetics: 0.36 +/- 0.01 vs 0.28 +/- 0.01 mmol p-nitrophenolate/h per g hemoglobin (Hb), P < 0.001; type 2 diabetics: 0.35 +/- 0.01 vs 0.28 +/- 0.01 mmol p-nitrophenolate/h per g Hb, P < 0.001). Insulin, at concentrations above physiological levels (1 mIU/ml), inhibited the PTP activities in erythrocytes from normal subjects (-15 +/- 4.1%, P < 0.01). Insulin could also modulate glycolysis, probably as a consequence of receptor tyrosine kinase activation, inducing phosphorylation of protein band 3 and hence the release of glycolytic enzymes. We have previously reported that a reductase enzyme in human erythrocytes is dependent on glycolysis being significantly activated (+28 +/- 3.1%, P < 0.001) by high insulin levels (1 mIU/ml). Mean basal reductase activities were found to be significantly lower in diabetics than in normal subjects (type 1 diabetics: 0.77 +/- 0.03 vs 0.97 +/- 0.02 mmol ferrocyanide/20 min per l cells, P < 0.001; type 2 diabetics: 0.77 +/- 0.04 vs 0.97 +/- 0.02 mmol ferrocyanide/20 min per l cells, P < 0.001), indicating altered erythrocyte metabolism in the diabetic patients. High glucose levels were used to mimic hyperglycemia condition, using erythrocytes from normal subjects. At 30 mM glucose, erythrocytic phosphatase activity was stimulated (+32 +/- 4.2%, P < 0.0001), although no effect was observed on the reductase enzyme at the same glucose levels. Results indicated that diabetic disorders appear to be associated with quantitative alterations of erythrocyte acid phosphatase activity and other enzymes that depend on the glycolytic rate (reductase). The overall data suggest that erythrocyte acid phosphatase may have a role in the modulation of glycolytic rates through the control of insulin receptor phosphorylation.

Topics: Acid Phosphatase; Adult; Blood Glucose; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Erythrocytes; Female; Glucose; Glycated Hemoglobin; Humans; Insulin; Kinetics; Male; Middle Aged; NADH, NADPH Oxidoreductases; Protein Tyrosine Phosphatase, Non-Receptor Type 1; Protein Tyrosine Phosphatases; Reference Values

Mesenteric arteries were isolated from the spontaneous diabetic BB rats, non diabetic BB rats and regular Wistar control rats. Gross morphology indicated that the mesenteric vascular bed of the control Wistar rats had a normal development of mesenteric fat pad around the vessels, while that of the diabetic BB rats showed drastically reduced perivascular fat pad, suggesting greater mobilization of fat for energy consumption in the hyperglycemic state of diabetes mellitus. The perivascular mesenteric fat pad of the non-diabetic BB rats was intermediate between those of the Wistar control and diabetic BB rats. The wet weight of the mesenteric arteries following removal of fat, vein and connective tissues was significantly greater in diabetic BB rats than in the corresponding controls. Microsomal membranes isolated from the mesenteric arteries of diabetic BB rats showed increased alkaline phosphatase and 5'-nucleotidase activities compared to those isolated from the two groups of non-diabetic control rats. Acid phosphatase activities were higher in both BB rat groups compared to the Wistar group. The total Ca2+ uptake by the microsomes of mesenteric arteries in the presence of ATP was not different among three experimental groups, but the ATP dependent active transport of Ca2+ was significantly increased and the passive Ca2+ binding was significantly reduced in diabetic group compared to the other two non-diabetic groups. Our results demonstrate that in the spontaneously diabetic BB rats, alterations in both structural and functional parameters may underline the vascular complications associated with type I diabetes mellitus in humans.

Topics: 5'-Nucleotidase; Acid Phosphatase; Adenosine Triphosphate; Alkaline Phosphatase; Animals; Biological Transport; Ca(2+) Mg(2+)-ATPase; Calcium; Cell Membrane; Diabetes Mellitus, Type 1; Electron Transport Complex IV; Male; Mesenteric Arteries; Microsomes; Muscle, Smooth, Vascular; NADH, NADPH Oxidoreductases; NADPH-Ferrihemoprotein Reductase; Organ Size; Phosphodiesterase I; Phosphoric Diester Hydrolases; Rats; Rats, Inbred BB; Rats, Wistar

Low molecular weight acid phosphatase encoded by the highly polymorphic locus ACP1 is a member of the protein-tyrosin phosphatase family (PTPases) which plays an essential role in the control of receptor signalling through phosphotyrosine pathways. Recent experiments have shown that purified rat liver ACP, corresponding to human ACP1, is able to hydrolyze a phosphotyrosine-containing synthetic peptide corresponding to the 1146-1158 sequence of the human insulin receptor, and shows a high affinity for it. This prompted us to analyze the degree of glycemic control in relation to ACP1 genetic variability in a sample of 214 diabetic pregnant women including IDDM, NIDDM and gestational diabetes. The ACP1 genotype was also determined in 482 non-diabetic pregnant women. In diabetic women glycemic levels in the last trimester of pregnancy appear to be significantly associated with the ACP1 genotype, and correlate positively with ACP1 enzymatic activity. The data suggest that quantitative variations of ACP1 may influence the clinical manifestations of diabetic disorders, and call for further studies on the role of this enzyme in the modulation of insulin-receptor phosphotyrosine pathways.

Topics: Acid Phosphatase; Blood Glucose; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetes, Gestational; Female; Genetic Variation; Genotype; Humans; Molecular Weight; Pregnancy; Pregnancy in Diabetics

Previous studies suggest that low bone mass is a potential complication of insulin-dependent diabetes mellitus. Nevertheless, the factors that influence diabetic osteopenia are not well established. In order to evaluate the prevalence and magnitude of diabetic osteopenia and its association with clinical and metabolic variables, we studied 94 consecutive patients with insulin-dependent diabetes mellitus. Their age ranged from 20 to 56 years and duration of diabetes varied from 1 to 35 years. Bone mineral density (BMD) was measured by dual X-ray absorptiometry at lumbar spine and proximal femur and the values were expressed as z-score. The presence and extent of microvascular complications, degree of metabolic control, and other risk factors for osteoporosis were recorded and some biochemical markers of bone metabolism were assessed. Diabetic patients showed reduced BMD in all sites (lumbar spine: -0.89 +/- 1.21; femoral neck: -0.99 +/- 1.24; Ward triangle: -1.05 +/- 1.24; P < 0.0001). Of the 94 patients 19.1% met diagnostic criteria for osteoporosis. BMD correlated with body mass index in all sites and with the duration of disease in Ward's triangle. Presence and extent of diabetic complications were associated with lower BMD, as was smoking. No correlation was found between BMD and biochemical markers. In conclusion, osteopenia is a common complication in patients with insulin-dependent diabetes mellitus. Microvascular complications are a critical point in the progression of diabetic osteopenia. Other risk factors for osteoporosis (nutritional status and smoking) must be taken into account.

Topics: Absorptiometry, Photon; Acid Phosphatase; Adult; Alkaline Phosphatase; Bone Density; Calcium; Diabetes Mellitus, Type 1; Female; Femur; Humans; Isoenzymes; Lumbar Vertebrae; Male; Middle Aged; Osteocalcin; Parathyroid Hormone; Spain; Tartrate-Resistant Acid Phosphatase

Topics: Acid Phosphatase; Albuminuria; Alkaline Phosphatase; Biomarkers; Bone Resorption; Diabetes Mellitus, Type 1; Glycated Hemoglobin; Humans; Hydroxyproline

Topics: Acid Phosphatase; Adolescent; Adult; Diabetes Mellitus, Type 1; Female; Histocytochemistry; Humans; Male; Microscopy, Electron; Monocytes; Peroxidase

Cytochemical studies have been performed on peripheral blood lymphocytes of 68 diabetic subjects, with various conditions of metabolic control, and 15 newly diagnosed insulin-dependent diabetic patients. 20 patients of the 1 group had diabetic retinopathy. In diabetic patients periodic acid Schiff positivity, acid phosphatase, and N-acetyl-beta-glucosaminidase activities of lymphocytes are fairly impaired, particularly in insulin-dependent diabetes. Concerning the alpha-naphthyl-acetate-esterase activity, the percentage of positive cells with coarse granules is significantly reduced (p less than 0.001) in diabetic patients as compared to controls, without difference related to age and sex. These abnormalities are more evident in patients with poor glyco-metabolic control. In patients with newly diagnosed insulin-dependent diabetes we have found a further decrease in alpha-naphthyl-acetate-esterase activity, and an increase in acid phosphatase and N-acetyl-beta-glucosaminidase activities. Cyto-enzymatic activities are not significantly different in subjects with diabetic retinopathy. The results of peripheral lymphocyte enzymatic activities in diabetics could be related to a depression of the cell-mediated immunity and could enhance the infections risk of these patients. Furthermore our data show an altered immunological balance in subjects with newly diagnosed type I diabetes.

Topics: Acid Phosphatase; Adult; Aged; Diabetes Mellitus; Diabetes Mellitus, Type 1; Diabetic Retinopathy; Female; Hexosaminidases; Histocytochemistry; Humans; Lymphocytes; Male; Middle Aged; Naphthol AS D Esterase; Periodic Acid-Schiff Reaction

Although reduced acid beta-glucosidase activity appears to be the primary enzyme defect in type I Gaucher disease, patients with this disorder also have marked elevation of serum acid phosphatase and beta-hexosaminidase activities but with a normal level of lactic dehydrogenase activity. Moreover, there is a characteristic alteration in the hexosaminidase isozyme distribution with a striking increase in hexosaminidase B. Since these changes appear to be consistent and unlike those associated with other disorders or the hormonally induced alterations associated with pregnancy, routine serum testing for the Tay-Sachs carrier state may offer a useful approach for the presumptive diagnosis and screening for Gaucher disease. Unlike the changes in affected homozygotes, there are no characteristic alterations of acid phosphatase or hexosaminidase in heterozygotes for Gaucher disease.

Topics: Acid Phosphatase; Diabetes Mellitus, Type 1; Female; Gaucher Disease; Genetic Carrier Screening; Hexosaminidases; Humans; Pregnancy; Tay-Sachs Disease

Nine genetic polymorphic systems (ACP1, PGM1, ADA, AK, G-6-PD, Hp, ABO, Rh, MN), were studied in a series of 138 subjects affected by JOD. Differences between diabetic patients and controls were observed in the distribution of phenotypes of the red cell acid phosphatase (ACP1), and the ABO and MN blood groups.

Topics: Acid Phosphatase; Blood Group Antigens; Child; Child, Preschool; Diabetes Mellitus, Type 1; Erythrocytes; Female; Gene Frequency; Humans; Infant; Male; Phenotype; Polymorphism, Genetic; Sex Factors

Studies have been carried out on activities of lysosomal beta-N-acetylhexosaminidase (hex), beta-galactosidase (beta-gal), alpha-glucosidase (alpha-glu), and acid phosphatase (AP) in serum and urine from patients with juvenile diabetes and matched controls. There is a large increase in blood and urinary hex activity (the former presenting three distinct patterns of abnormality), a moderate increase in urinary beta-gal, and a small increase in urinary alpha-glu activity, but no elevation of blood or urinary AP in the diabetics. Urinary alpha-glu activity in the diabetics shows striking inhibition by glucose, and this may reflect a similar phenomenon in vivo. Although glycohydrolase activities are elevated in patients with no detectable microangiopathy, more striking changes may be observed in patients with severe small-vessel disease. These alterations may be associated with increased glycoprotein catabolism in the diabetic, an area in need of further studies in the human and experimental diabetic animal.

Topics: Acid Phosphatase; Adolescent; Adult; Diabetes Mellitus, Type 1; Drug Stability; Female; Galactosidases; Glucose; Glucosidases; Glycoside Hydrolases; Hexosaminidases; Humans; Lysosomes; Male; Sex Factors