Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Phosphotyrosine protein phosphatases and diabetic pregnancy: an association between low molecular weight acid phosphatase and degree of glycemic control. 862 Sep 37

This paper discusses management of hyperglycemia in minority children with type 2 diabetes mellitus (DM). Over the past several years the incidence of type 2 DM in minority children and adolescents has markedly increased. Intensive management of children with type 2 DM includes exercise, diet, insulin therapy, oral drug (metformin) therapy, and combination insulin-oral drug therapy. The results of a study of the efficacy of treatment modalities in 35 African-American children are presented. In the study, the patients were divided into two groups, one treated with diet or metformin therapy (20 children) and the other with insulin or a combination of insulin and metformin (15 children). All of the children in the study were negative for antibodies to glutamic acid decarboxylase. Plasma glucose and serum C-peptide concentrations were measured at 0, 30, 60, 90, and 120 min after ingestion of a liquid meal (Sustacal) (7 ml/kg with a maximum of 360 ml). The increase of C-peptide (ACP) in response to the mixed meal was calculated by peak minus fasting C-peptide. ACP was significantly higher in those children treated with diet/metformin than in those treated with insulin/insulin and metformin combination therapy (4.6 +/- 1.9 vs 21 +/- 1.6, p <0.01). Mean HbA1c at one-year follow up was lower for the diet/metformin patients than in the insulin/insulin and metformin group (7.0 +/- 2.8 vs 11.4 +/- 3.7, p <0.01). Our results indicate that in children with type 2 DM, there is more severe pancreatic beta-cell dysfunction in the group of children requiring insulin therapy.
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PMID:Management of hyperglycemia in minority children with type 2 diabetes mellitus. 1201 28

We have previously demonstrated abnormalities in insulin secretion in adolescents with type 2 diabetes mellitus (DM2) in response to the mixed meal test and to glucagon. In order to further assess beta-cell function in DM2, we measured insulin and C-peptide responses to oral glucose in adolescents with DM2 in comparison to non-diabetic obese and lean adolescents. We studied 20 patients with DM2, 25 obese adolescents with matching body mass index (BMI) (33.8 +/- 1.4 vs 34.3 +/- 1.0 kg/m2), and 12 non-obese control adolescents (BMI 22.6 +/- 0.6 kg/m2). Mean age, sex and sexual maturation did not differ between the three groups. All adolescents with DM2 had negative islet cell antibodies (ICA); five patients were on diet and 15 on insulin treatment. Fasting lipid profiles were determined in all participants. Plasma glucose and serum C-peptide and insulin levels were measured at 0, 30, 60, 90, and 120 min after an oral glucose load. The C-peptide increment (deltaCP) was calculated as peak minus fasting C-peptide. Area under the curve (AUC) was estimated using the trapezoid method. Insulin resistance was estimated using the HOMA model (HOMA-IR). The first phase of insulin secretion (PH1) was computed using a previously published formula. Serum triglyceride levels were significantly higher in the patients with DM2 compared to the non-obese controls (1.4 +/- 0.1 vs 0.9 +/- 0.1 mmol/l; p = 0.02). Plasma glucose AUC was greater in the patients with DM2 compared to the obese and non-obese control groups (1,660 +/- 130 vs 717 +/- 17 vs 647 +/- 14 mmol/l x min; p < 0.0001). ACP was lower in adolescents with DM2 than in obese and non-obese adolescents (761 +/- 132 vs 1,721 +/- 165 vs 1,225 +/- 165 pmol/l; p < 0.001). Insulin AUC was lower in the patients with DM2 compared to obese controls (888 +/- 206 vs 1,606 +/- 166 pmol/l x h; p = 0.009), but comparable to that of the non-obese controls (888 +/- 206 vs 852 +/- 222 pmol/l x h; p = 0.9). Insulin AUC was also higher in the obese than in the non-obese group (p = 0.05). PH1 was significantly higher in the obese group compared to the patients with DM2 as well as to the non-obese controls (2,614 +/- 2,47.9 vs 929.6 +/- 403.5 vs 1,946 +/- 300.6 pmol/l, respectively; p = 0.001). PH1 was also higher in the non-obese controls than in the patients with DM2 (p = 0.05). HOMA-IR was three-fold higher in the patients with DM2 than in the BMI-matched obese group, and five-fold higher than in the lean controls (14.3 +/- 1.2 vs 5.4 +/- 0.8 vs 2.9 +/- 0.4; p = 0.0002). Adolescents with DM2 have dyslipidemia, a significant cardiovascular risk factor. Decreased beta-cell function is characteristic of adolescents with DM2 in the presence of severe insulin resistance.
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PMID:Type 2 diabetes mellitus in African-American adolescents: impaired beta-cell function in the face of severe insulin resistance. 1656 86

Objective: This study evaluated whether there is a difference in the proportion of patients with type 2 diabetes who achieve a hemoglobin A1c (HbA1c) <7% within one year following treatment by an endocrinologist or primary care physician (PCP). Methods: We conducted a retrospective, propensity-matched study of patients with type 2 diabetes that were not optimally controlled and seen within our health system from 2007-2016. We assessed differences in short term health outcomes for patients following an endocrinologist visit compared to a PCP visit. Results: Patients seen by endocrinologists obtained HbA1c control at a faster rate (hazard ratio = 1.226; 95% confidence interval = 1.01 to 1.488) than those seen by a PCP. Furthermore, 34.5% and 29.5% of those treated by endocrinologists and PCPs, respectively, obtained HbA1c control by one year. Endocrinologists were more likely to prescribe a new medication class within 90 days than PCPs (14.1% versus 10.3%, respectively, P = .043). There was no difference in the risk of hospitalization between groups; 24.4% and 24.1% of those treated by endocrinologists and PCPs, respectively, were hospitalized within one year. Conclusion: Patients treated by endocrinology specialists were more likely to achieve a target HbA1c of <7% (53 mmol/mol) than those treated by PCPs in our health-care system. The performance difference may be partially explained by a higher rate of adding new classes of diabetes medications to the patient's pharmacologic regimens within 90 days by endocrinologists compared with PCPs. The long-term impact of these differences is unknown but has the potential to have an unfavorable impact on the health of the population. Abbreviations: ACP = American College of Physicians; CI = confidence interval; DUHS = Duke University Health System; HbA1c = hemoglobin A1c; HR = hazard ratio; PCP = primary care physician; SMD = standard mean difference.
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PMID:DIFFERENCES IN ACHIEVING HBA1C GOALS AMONG PATIENTS SEEN BY ENDOCRINOLOGISTS AND PRIMARY CARE PROVIDERS. 3072 Mar 49