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Biomedical subjects

J Buse

Publications and source records attributed to J Buse.

16 recordsLinked to original sources
PubMed2005

The metabolic syndrome: time for a critical appraisal. Joint statement from the American Diabetes Association and the European Association for the Study of Diabetes.

BACKGROUND: The term 'metabolic syndrome' refers to a clustering of specific cardiovascular disease (CVD) risk factors whose underlying pathophysiology is thought to be related to insulin resistance. METHODS: Since the term is widely used in research and clinical practice, we undertook an extensive review of the literature in relation to the syndrome's definition, underlying pathogenesis, association with cardiovascular disease and to the goals and impact of treatment. DISCUSSION: While there is no question that certain CVD risk factors are prone to cluster, we found that the metabolic syndrome has been imprecisely defined, there is a lack of certainty regarding its pathogenesis, and there is considerable doubt regarding its value as a CVD risk marker. Our analysis indicates that too much critically important information is missing to warrant its designation as a 'syndrome'. CONCLUSION: Until much-needed research is completed, clinicians should evaluate and treat all CVD risk factors without regard to whether a patient meets the criteria for diagnosis of the 'metabolic syndrome'.

Body Mass Index↗
PubMed2000

Combining insulin and oral agents.

Type 2 diabetes mellitus is a progressive disorder, and maintenance of near-normal glycemic control has been demonstrated to reduce the risk of its associated long-term vascular complications. This treatment goal can be achieved in most patients with use of single oral agents, combinations of oral agents, or insulin. Secondary failure rates for intensive oral or injected therapy are high, however, especially in patients with long-standing disease. A substantial body of evidence indicates that combination therapy with insulin and oral antidiabetic agents can safely establish excellent glycemic control in most patients, while it reduces the required dosage of insulin and, in some combinations, mitigates the weight gain associated with insulin therapy. The availability of more convenient insulin-delivery systems may render the addition of insulin to oral drug therapy more acceptable to patients and clinicians. The most-studied combination is that of insulin and the sulfonylurea drugs. Randomized, prospective clinical trials have documented the benefits of thiazolidinediones, metformin, and acarbose in combination with insulin. To date, however, clinical trial data are insufficient for use in determining the optimal combination of agents, insulin formulations, and dosages among the many currently available possibilities.

Administration, Oral↗
PubMed1996

The GENNID Study. A resource for mapping the genes that cause NIDDM.

OBJECTIVE: To develop a resource, consisting of comprehensive data and lymphoblastoid cell lines, of well-characterized NIDDM families that will be available to the scientific community for genetic studies of NIDDM. RESEARCH DESIGN AND METHODS: Non-Hispanic white, Hispanic, African-American, and Japanese-American multiplex NIDDM families, with a minimum of one affected sib-pair, are being collected by the eight Harold Rifkin Family Acquisition Centers. Detailed family and medical histories are obtained from all participants. Family members with diabetes have fasting blood samples drawn, while nondiabetic family members have an oral glucose tolerance test and, when possible, insulin sensitivity and insulin secretion measurements by frequently sampled intravenous glucose tolerance testing or euglycemic insulin clamp. Lymphoblastoid cell lines are established for all participants. RESULTS: Over 1,400 individuals from approximately 220 families have been studied since the start of the GENNID (Genetics of NIDDM) program in July 1993. The goal is that by July 1997, data from 300 non-Hispanic white families, > 100 Hispanic families, > 100 African-American families, and 15 Japanese-American families will have been collected. CONCLUSIONS: The identification of the genes responsible for NIDDM may now be achievable, but only if sound phenotypic data are linked to genetic material from a large number of well-described multiplex families. The GENNID project of the American Diabetes Association is creating a comprehensive resource that will expedite the identification of the genetic basis of NIDDM.

Black or African American↗
PubMed1991

Cystic fibrosis transmembrane regulator mRNA expression relative to ion-nutrient transport in spontaneously differentiating human intestinal CaCo-2 epithelial cells.

The relative abundance of cystic fibrosis transmembrane regulator (CFTR) message at various stages of postconfluence development was compared with evolving cellular ion-nutrient transport properties of CaCo-2 human intestinal cells. Initially these cells demonstrate electrogenic Cl secretion manifested by secretagogue-induced changes in short-circuit current. Over time, however, the secretory characteristics of CaCo-2 monolayers diminish, and brush border hydrolase activities and glucose-dependent and amiloride-sensitive Na transport increase. With a polymerase chain reaction-derived cDNA probe to CFTR exon 13, two distinct mRNA transcripts of 6.5 and 4.3 kb were found. No significant differences in their abundance were noted in cells at 6 and 28 days after confluence. These data suggest two possible interpretations for the role of CFTR protein. First, if CFTR is membrane Cl channel, its protein expression or activity could be differentially regulated during CaCo-2 cell development. Alternatively, CFTR may not be a Cl channel but may serve as an important regulatory membrane protein.

Amiloride↗
PubMed1983

Lymphocyte abnormalities in the BB rat.

The BB rat has a marked T cell lymphocytopenia, with a near absence of peripheral "helper" T cells recognized by monoclonal antibody W3/25 (W3/25+ T cells). The lymphocytes of the BB rat's spleen and thymus were examined for the presence of W3/25+ T cells, which were found to be absent in the spleen but present in normal amounts in the thymus. Concanavalin A (Con A) responsiveness was absent in the BB's peripheral blood and spleen but present in the thymus. Thus, in these three lymphoid compartments, Con A responsiveness directly correlated with the presence or absence of W3/25+ T cells. These lymphocyte abnormalities in the BB rat are notably different from lymphocyte changes present in human type I diabetes.

Animals↗
PubMed1981

Kallikrein-induced uterine contraction independent of kinin formation.

Responses of smooth muscle to kallikreins (EC 3.4.21.8) are generally considered to result from kinin formation. This premise was reexamined with the isolated rat uterus. Rat urinary kallikrein or bradykinin produced dose-dependent contractions of rat uterus but kallikrein was 5-fold more potent than bradykinin. Kallikrein caused an immediate series of rhythmic contractions which could be increased gradually with subsequent addition of kininogen substrate. Kallikrein-induced contractions were unaffected by carboxypeptidase B or a bradykinin antiserum whereas bradykinin-induced contractions were attenuated or abolished. Other serine proteinases, including trypsin, either did not induce contraction in the absence of added kininogen or did so minimally. Although small amounts of kininogen-like substrate were found in uterine tissue, detectable kinin levels (greater than 4 pg) could not be found in bathing media during maximal kallikrein-induced contractions or after uterine tissue was incubated with high concentrations of the enzyme in the presence of SQ 20881, a kininase II inhibitor. The data suggest that uterine contraction produced by a homologous kallikrein does not involve kinin formation but results from an action of this serine proteinase upon other accessible systems coupled to the contractile response.

Animals↗
PubMed1977

Hyperinsulinemic hypoglycemia: effect of epinephrine suppression.

The inhibitory effect of epinephrine on basal and tolbutamide-stimulated insulin release was studied in 5 patients with hyperinsulinemic hypoglycemia. Epinephrine inhibited both basal and tolbutamide-induced insulin release in patients with beta-cell adenoma and hyperplasia, but failed to inhibit insulin release in a patient with beta-cell carcinoma. The inhibition of basal insulin with epinephrine was maximum in patients with beta-cell hyperplasia. This differential inhibitory effect of epinephrine on insulin release may prove to be a useful screening test in the preoperative diagnosis of the nature of the lesion producing hyperinsulinemia.

Adenoma↗
PubMedDate not supplied

The PROTECT Study: final results of a large multicenter postmarketing study in patients with type 2 diabetes. Precose Resolution of Optimal Titration to Enhance Current Therapies.

The Precose Resolution of Optimal Titration to Enhance Current Therapies (PROTECT) trial was a nationwide postmarketing study designed to assess the effectiveness, tolerability, and safety of acarbose in patients with type 2 diabetes mellitus. This prospective, multicenter, open-label, 28-week trial enrolled 6142 patients who had type 2 diabetes that was inadequately controlled with either diet alone or diet plus a sulfonylurea. The dosage of acarbose was titrated from 25 mg TID to 50 mg TID (forced titration) and then titrated from 50 mg TID to 100 mg TID based on tolerability and efficacy. Efficacy of glycemic control was assessed by recording changes in glycated hemoglobin A1c (Hb A1c) and 1-hour postprandial plasma glucose (PPG) levels. Tolerability and safety were determined on the basis of patients' reports of treatment-emergent adverse events and by review of laboratory test results. Acarbose was safe and effective in improving glycemic control in patients with type 2 diabetes, regardless of their age, weight, ethnic background, time since diagnosis, or concomitant sulfonylurea therapy. Hb A1c levels declined throughout the treatment period, for a mean change in Hb A1c of -0.66%. The mean change from baseline in 1-hour PPG levels was -41 mg/dL at the end of treatment. Although all types of patients enrolled in the study responded positively to acarbose therapy, certain subgroups responded particularly well, especially those who had been diagnosed with the disease for less than 1 year and those who were untreated at study entry. Adverse events consisted primarily of gastrointestinal disturbances.

Acarbose↗