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Biomedical subjects

M B Davidson

Publications and source records attributed to M B Davidson.

At least 37 records · Page 2Linked to original sources
PubMed1998

Application of a diabetes managed care program. The feasibility of using nurses and a computer system to provide effective care.

OBJECTIVE: Treatment of patients with diabetes often falls short of recommended process and outcome guidelines. To improve the quality of the provided diabetes care, a program (the Comprehensive Diabetes Care Service [CDCS]) using a computerizing tracking and recall system in conjunction with nurses following protocols was implemented in a managed care setting. The impact of this program was studied and compared to the care provided to patients in another managed care setting. RESEARCH DESIGN AND METHODS: Patients followed in the CDCS who completed a diabetes education course were compared with patients followed in a group model health maintenance organization (GMH) who also completed a diabetes education course. CDCS patients received routine care in the program. GMH patients came to the CDCS yearly to have a diabetes evaluation. A chart review was also performed on their GMH outpatient records. RESULTS: Initial HbA1c levels were higher in the CDCS group than in the GMH group (median of 11.9 vs. 10.0%). In the CDCS patients, HbA1c levels not only fell significantly but were also significantly lower (P < 0.05) than in the GMH patients during the 2nd and 3rd year of follow-up care. There were no significant changes in HbA1c levels in the GMH patients. When CDCS patients were divided into compliant and noncompliant patients, the median HbA1c levels in compliant patients was 8.2%, compared with 11.5% in the noncompliant group. The CDCS patients who needed treatment for hypercholesterolemia were more likely to have a lowering of their cholesterol levels than the GMH patients. All process measures, such as yearly measurement of HbA1c levels, lipid levels, and foot and retinal exams, occurred much more frequently in the CDCS patients. CONCLUSIONS: The system developed and implemented for managing diabetes improved both outcome and process measures. The comparison group, followed at another managed care setting, received the care consistent with the average (suboptimal) quality of care provided to patients with diabetes in the U.S. Therefore, by using innovative systems of management, the treatment of patients with diabetes can be greatly improved.

Adult↗
PubMed1997

An overview of metformin in the treatment of type 2 diabetes mellitus.

Type 2 diabetes mellitus results from impaired insulin secretion and reduced peripheral insulin sensitivity. Treatment options include diet, oral antihyperglycemic agents, and insulin. Metformin, an oral biguanide, ameliorates hyperglycemia by improving peripheral sensitivity to insulin, and reducing gastrointestinal glucose absorption and hepatic glucose production. Unlike sulfonylureas, it does not stimulate insulin secretion, aggravate hyperinsulinemia, or cause hypoglycemia or weight gain (weight stabilizes or decreases). It also has beneficial effects on serum lipid profiles. In lean or overweight type 2 diabetic patients uncontrolled by diet, metformin monotherapy significantly improves glycemic control, compared with placebo, and to similar extents as sulfonylurea monotherapy. In secondary sulfonylurea failure, combination metformin-sulfonylurea treatment significantly improves glycemic control beyond that achieved with either agent along. Metformin-sulfonylurea also appears to be as effective as insulin or insulin plus sulfonylurea, suggesting that such combination therapy may obviate or substantially delay insulin therapy. Limited data suggest that metformin-insulin therapy may improve glycemic control, possibly reducing insulin requirements, in type 2 diabetic patients uncontrolled by insulin alone following secondary sulfonylurea failure. Gastrointestinal side effects are common, but usually tolerated. Lactic acidosis risk is minimal, provided that contraindications, particularly renal impairment, and prescribing guidelines are respected. Aside from elevated plasma metformin levels with cimetidine and synergistic hypoglycemia with sulfonylureas, few interactions occur. Thus, metformin is safe and effective both as monotherapy or in combination with other antihyperglycemic agents in type 2 diabetic patients requiring additional glycemic control and may be advantageous when weight control is desirable and/or hyperlipidemia exists.

Diabetes Mellitus, Type 2↗
PubMed1997

Human stanniocalcin inhibits renal phosphate excretion in the rat.

Stanniocalcin (STC) is a glycoprotein hormone first identified in bony fishes where it counteracts hypercalcemia by inhibiting gill calcium uptake and stimulating renal inorganic phosphate (Pi) reabsorption. Human STC (hSTC) has recently been cloned and sequenced and is highly homologous to the fish hormone at the amino acid level. The objective of this study was to examine the possible effects of hSTC on electrolyte homeostasis and renal function in the rat. Recombinant hSTC was expressed in bacteria and purified by metal-ion affinity chromatography and reverse-phase high performance liquid chromatography. Anesthetized animals were given bolus infusions of 1, 5, or 10 nmol hSTC per kilogram of body weight. Control animals received solvent alone. The most effective dosage was 5 nmol/kg, which caused significant reductions in both absolute and fractional phosphate excretion in comparison with control rats. The hSTC had no effect on the renal excretion of other ions, the glomerular filtration rate, renal blood flow, blood pressure, or plasma electrolytes (Na+, K+, Ca2+, Pi, Mg/+). The maximum effect of hSTC on phosphate excretion was observed 60-80 minutes postinjection. Lesser effects were obtained with higher and lower dosages of hormone. When renal cortical brush-border membrane vesicles were isolated from control and hormone-treated animals 80 minutes postinjection, the rate of Na+/Pi cotransport was found to be 40% higher in vesicles from hormone-treated animals (p < 0.01; 5 nmol hSTC/kg). Together, the renal clearance and membrane vesicle data indicate that hSTC participates in the renal regulation of Pi homeostasis in mammals.

Animals↗
PubMed1997

Diabetes management: improving care in HMO and community settings.

Developing an effective, quality-driven disease management program for the treatment of patients with diabetes has become essential for MCOs, which cover the majority of American individuals suffering from this condition. At Cedars-Sinai Medical Center in Los Angeles, the Diabetes Managed Care Program was developed and implemented in an effort to provide a model for similar diabetes management initiatives in both managed health care plans and community settings.

California↗
PubMed1996

A clinical approach for the diagnosis of diabetes mellitus: an analysis using glycosylated hemoglobin levels. Meta-analysis Research Group on the Diagnosis of Diabetes Using Glycated Hemoglobin Levels.

OBJECTIVE: To determine whether a glycosylated hemoglobin level can be used in place of an oral glucose tolerance test (OGTT) to diagnose diabetes. DATA SOURCES/STUDY SELECTION: An augmented MEDLINE search was performed to identify all reports from 1966 through June 1994 in which glycosylated hemoglobin levels were measured concurrently with performance of OGTTs in the same study. The corresponding authors were contacted and asked to provide individual data for all subjects tested. A total of 31 investigators representing 34 possible studies responded, and 18 were able to provide us with the data requested. Overall fasting plasma glucose concentrations, 2-hour postdextrose glucose concentrations, and glycosylated hemoglobin levels were available from 11 276 individuals. DATA EXTRACTION: To define normal glucose tolerance, impaired glucose tolerance (IGT), and diabetes, modified World Health Organization criteria were used. DATA SYNTHESIS: An analysis of the methods used for measurement of glycosylated hemoglobin levels revealed that the HbA1c assay showed the least variance in normal subjects. Therefore, only data from the 8984 subjects who had HbA1c levels measured were used. When we used the mean HbA1c level plus 4 SDs as a cutpoint, the sensitivity was 36% and specificity was 100% compared with the results of the OGTT. Because of the lack of agreement between OGTT results and HbA1c levels, models were created to analyze the distribution of HbA1c levels in each study. Using these models, we identified 3 subpopulations. The third subpopulation was likely to represent subjects with diabetes. When we applied an HbA1c level of 7.0% as a cutpoint, the sensitivity was 99.6% for the third subpopulation. When this cutpoint was reapplied to the OGTT results, of those subjects with an HbA1c level of at least 7.0%, 89% had diabetes, 7% had IGT, and 4% were normal. CONCLUSIONS: Although the OGTT is the "gold standard" for diagnosing diabetes, it is known to be poorly reproducible and is often not performed. Not only is use of an HbA1c level to diagnose diabetes more convenient, but therapeutic decisions are based on this value, regardless of the findings on the OGTT. An HbA1c level of 7.0% or higher often requires pharmacological intervention and is most often associated with the diagnosis of diabetes by World Health Organization standards. An HbA1c level below 7.0% would generally be treated with diet and exercise, regardless of the diagnosis of IGT or diabetes by OGTT. Thus, measurement of HbA1c levels may represent a reasonable approach to identifying treatment-requiring diabetes.

Diabetes Mellitus↗
PubMed1996

Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells.

It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. The effect of this cytokine on insulin action in muscle, which is responsible for 80% of the glucose disposal in the body, has not been studied. Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. However, there was a significant increase in basal transport in TNF-alpha- treated cells. Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. In cells cultured without insulin, basal transport was slightly increased and the insulin-stimulated increase in transport was decreased by approximately 60% but the cell protein was decreased by approximately 60%, suggesting cytotoxicity. Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. These results suggest that TNF-alpha affects glucose metabolism, causing increased basal uptake in muscle cells and decreased uptake in adipocytes. TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport.

3T3 Cells↗
PubMed1996

Dexamethasone-induced impairment in skeletal muscle glucose transport is not reversed by inhibition of free fatty acid oxidation.

Our previous studies suggested a possible role for the glucose-free fatty acid (FFA) cycle, ie, preferential utilization of FFA by muscle at the expense of glucose, in dexamethasone (DEX)-induced insulin resistance. To determine whether this resistance could be reversed by inhibiting FFA utilization, we used etomoxir, a potent inhibitor of mitochondrial FFA oxidation. Male Sprague-Dawley rats were injected subcutaneously with 1 mg/kg DEX or the vehicle every other day for 10 days, and half of each group was administered 10 mg/kg etomoxir by gavage once per day and 1 hour before the experiment. As expected, etomoxir treatment increased serum FFA levels and inhibited FFA oxidation by diaphragm in vitro. Administration of etomoxir decreased serum glucose and insulin concentrations under basal conditions in both control and DEX-treated animals, implying enhanced insulin sensitivity. DEX treatment significantly increased endogenous glucose production and decreased whole-body glucose disposal, as well as 2-deoxyglucose (2-DG) uptake by skeletal muscle during euglycemic-hyperinsulinemic clamps. Administration of etomoxir led to small but significant increases in glucose disposal rates of both control (14%) and DEX (23%) groups, but had no effect on residual endogenous glucose production. Thus, DEX-induced insulin resistance was marginally ameliorated but not completely reversed by etomoxir. Depressed 2-DG uptake by individual muscle tissues observed in the present study in conjunction with the absence of free intracellular glucose in muscle tissue following glucose-insulin infusion strongly suggests that the primary defect in glucose metabolism is at the level of transport. Neither overall abundance of the insulin-sensitive glucose transporter (GLUT-4) in skeletal muscle nor its distribution between intracellular stores and plasma membrane were modified by DEX treatment, either, under basal conditions or in response to acute insulin stimulus. These results suggest a defect(s) in the inherent activity of plasma membrane-bound GLUT-4 as the likely mechanism for DEX-induced insulin resistance.

Animals↗
PubMed1996

Maximal dose glyburide therapy in markedly symptomatic patients with type 2 diabetes: a new use for an old friend.

No consensus exists as to the best approach for treating markedly symptomatic patients with new-onset (or diet-treated) type 2 diabetes. Therefore, based on the experience of one successful case, further studies were undertaken to determine the safety and efficacy of maximal dose glyburide (10 mg, twice daily, in patients < 65 yr of age) or half the dose (10 mg, daily, in patients > or = 65 yr of age) for treating these patients. Fifty-five patients with polyuria, polydipsia, nocturia, involuntary weight loss, and blood glucose concentrations of 300 mg/dL or greater were treated following protocols that used maximal dose ( < 65 yr of age) or half-maximal dose ( > or = 65 yr of age) sulfonylurea agent therapy. Data were collected retrospectively in 30 patients and prospectively in 25. Patients in the prospective group differed only in that more laboratory measurements were obtained, and less strict guidelines for using insulin were adopted. Data were collected in both groups at baseline and 1 week and 4 months after starting the sulfonylurea agent therapy. Patients responded rapidly with a fall in blood glucose levels from 456 +/- 12 mg/dL at baseline to 202 +/- 10 mg/dL at 1 week to 120 +/- 5 mg/dL at 4 months. Glycated hemoglobin levels fell from 18.1 +/- 0.4% at baseline to 8.1 +/- 0.2% ( P < 0.0001) at 4 months. Most patients had symptomatic improvement within 3 days. Seventeen patients had positive (small or larger) urinary ketones, and 5 had positive serum ketones. Insulin to glucose and C peptide to glucose ratios improved maximally at 1 week, indicating rapid reversal of glucotoxicity on the beta-cell. At 4 months, 11 patients were receiving diet therapy alone, 29 were receiving submaximal dose sulfonylurea agent therapy, 6 remained on maximal dose sulfonylurea agent therapy, and only 3 were receiving insulin therapy. Six patients were lost to follow-up. No patient experienced hypoglycemia in the first 2 weeks of treatment. Maximal dose sulfonylurea agent therapy is a safe and effective method for treating patients with markedly symptomatic type 2 diabetes. Patients improve rapidly and are able to avoid the immediate institution of long term insulin therapy.

Adolescent↗
PubMed1996

Quality of outpatient care provided to diabetic patients. A health maintenance organization experience.

OBJECTIVE: To document the quality of diabetes care provided to patients in a large health maintenance organization (HMO) from 1 January 1993 to 1 January 1994 and compare it to the standards of the American Diabetes Association (ADA). RESEARCH DESIGN AND METHODS: To meet a Health Plan and Employer Data Information Set (HEDIS) requirement, a major HMO in California identified 14,539 members with diabetes and randomly selected 384 individuals for review. Charts were available on 353 of these patients, and after obtaining the information for the HEDIS review, additional information was extracted from the charts by an outside chart reviewer. This data set was used for an analysis of the quality of diabetic care provided by the participating medical groups to these HMO members during 1 year. Documentation of follow-up and measures of glycemic and lipid control was examined both for absolute values and for the frequency of measurement over the year. These results were compared to the ADA standards of care. RESULTS: Although patients averaged 4.5 visits to their primary care physicians (PCPs) over the year, 21% had one or fewer visits per year. Glycated hemoglobin levels were not documented in 56% of patients (ADA recommends two to four measurements per year), and of those with a glycated hemoglobin level measured. 39% had at least one value > or = 10%. Fasting plasma glucose concentrations were not documented in 65% of patients (four to six per year recommended). Foot exams (which should be performed at each regular visit) were not documented for 94% of patients. Urine protein measurements were not performed in 52% of patients. Additionally, many patients had elevated and untreated lipid abnormalities. CONCLUSIONS: In spite of the frequency of PCP visits during the year for many of these patients, diabetes management was inadequate. This lack of adequate preventive care will lead to an increased risk of the development of the acute and chronic complications of diabetes, creating an even greater future burden on the health care system and negative consequences for patients.

Body Weight↗
PubMed1995

Insulin resistance in rats harboring growth hormone-secreting tumors: decreased receptor number but increased kinase activity in liver.

Growth hormone (GH) is a potent antagonist of insulin action, and this resistance occurs primarily at a post-binding step(s). To elucidate the underlying mechanisms, the effects of chronic GH excess on the structure and function of insulin receptors partially purified from the liver were examined in rats harboring GH-secreting tumors. Insulin resistance was established in this animal model of GH hypersecretion by a hyperinsulinemic euglycemic clamp. Specific binding of 125I-insulin and receptor number were reduced in tumor animals by 40% and 62%, respectively, reflecting downregulation of the insulin receptor by hyperinsulinemia in these animals. Receptors from tumor animals showed a 50% increase in beta-subunit phosphorylation and in the kinase activity toward the synthetic polypeptide Glu4:Tyr1 when measured in vitro in the absence of insulin; however, the incremental stimulation by insulin (170 nmol/L) of the phosphorylation of either the beta-subunit or Glu4:Tyr1 was not different between control and experimental animals. There was no difference between the two groups in Glu4:Tyr1 phosphorylation measured after immunodepletion of receptors by antibodies to the insulin receptor, indicating that the observed alteration in the kinase activity of tumor animals was intrinsic to the insulin receptor. Exposure to chronic GH excess did not alter insulin receptor structure, as evidenced by electrophoretic mobility under reducing and nonreducing conditions. The enhanced basal kinase activity of the receptor from tumor animals may reflect a more highly phosphorylated state of the receptor (and hence elevated enzyme activity) in these animals due to elevated serum insulin levels. These results demonstrate that the hepatic insulin resistance in rats chronically exposed to GH excess is not due to impaired insulin receptor kinase activity.

Animals↗
PubMed1995

Clinical implications of insulin resistance syndromes.

Epidemiologic studies have shown an association between higher insulin levels and coronary artery disease, and metabolic studies have associated insulin resistance and compensatory hyperinsulinemia with hypertension, obesity, and lipid disorders. This review focuses on the clinical implications (rather than the metabolic pathogeneses) of these associations and how practicing physicians should manage patients with insulin resistance.

Coronary Disease↗
PubMed1995

Response to Nathan.

Explore the source record for details and available documents.

Diabetes Complications↗
PubMed1995

Management of patients with diabetes by nurses with support of subspecialists.

A program was developed for managing diabetic patients within an HMO system. The system uses physician-supervised diabetes nurse specialists and a computer system to enhance compliance and management of patients. The focus of the program is on preventing hospitalizations as well as preventing the development of the complications of diabetes, with early detection (and treatment) of any complications that do occur. The program was associated with a significant fall in glycated hemoglobin levels (12.5% to 9.5%, p < 0.005) and led to likely cost-savings by avoiding acute hospitalizations for diabetes in an estimated 244 patients over a 4-year period.

California↗