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F Vinicor

Publications and source records attributed to F Vinicor.

At least 55 records · Page 3Linked to original sources
PubMed1992

Trends in diabetes and diabetic complications, 1980-1987.

OBJECTIVE: Although diabetes is a major source of morbidity and mortality in the United States, only recently has a unified national surveillance system begun to monitor trends in diabetes and diabetic complications. RESEARCH DESIGN AND METHODS: We established a diabetes surveillance system using data for 1980-1987 from vital records, the National Health Interview Survey, the National Hospital Discharge Survey, and the Health Care Financing Administration's records to examine trends in the prevalence and incidence of diabetes, diabetes mortality, hospitalizations, and diabetic complications. RESULTS: From 1980 through 1987, the number of individuals known to have diabetes increased by 1 million--to 6.82 million. Age-standardized prevalence for diabetes increased 9% during this period, from 25.4 to 27.6/1000 U.S. residents (P = 0.03). The incidence of diabetes increased among women (P = 0.003), particularly among those greater than 65 yr old (P = 0.02). Age-standardized mortality rates (for diabetes as either an underlying or contributing cause) per 100,000 individuals with diabetes declined 12%, from 2350 to 2066. Annual mortality rates from stroke (as an underlying cause and diabetes as a contributing cause) and diabetic ketoacidosis declined 29% (P = 0.003) and 22% (P less than 0.001), respectively. During these 8 yr, hospitalization rates for major CVD and stroke (as the primary diagnoses and diabetes as a secondary diagnosis) increased 34% (P = 0.006) and 38% (P = 0.01), respectively. Also during this period, hospitalization rates increased 21% for diabetic ketoacidosis (P = 0.01) and 29% for lower-extremity amputations (P = 0.06). From 1982 through 1986, treatment for end-stage renal disease related to diabetes increased greater than 10% each year (P less than 0.001). The prevalence of diagnosed diabetes was nearly twice as high in blacks as in whites (P = 0.04). Blacks also had increased rates of lower-extremity amputation (P = 0.02), diabetic ketoacidosis (P less than 0.001), and end-stage renal disease (P = 0.01). CONCLUSIONS: Diabetes surveillance data will be useful in planning, targeting, and evaluating public health efforts designed to prevent and control diabetes and its complications.

Amputation, Surgical↗
PubMed1990

Economic impact of diabetes mellitus in the elderly.

Diabetes mellitus is a prevalent disease in Americans aged 65 years and older. It leads to significant morbidity, mortality, and utilization of health care services. Using extant data, we estimated that health care services provided to elderly persons with diabetes cost $5.16 billion annually, nearly 80% of which were attributed to hospital costs. Treatment for cardiovascular disease as a complication of diabetes accounted for the largest proportion of these costs. In addition to admissions for uncomplicated diabetes, substantial portions of inpatient costs were attributed to renal and neurologic diseases. Expenditures per capita for medical care were 50% higher in the elderly diabetic population than in an elderly nondiabetic population. The average yearly expenditure per diabetic patient was estimated to be $4265, $900 of which were out-of-pocket expenses. We conclude that increased vigilance to prevent or delay the incidence of morbidity leading to hospital admissions must take priority in caring for patients with DM. Intensifying outpatient care may offer the opportunity to accomplish this goal.

Aged↗
PubMed1987

DIABEDS: a randomized trial of the effects of physician and/or patient education on diabetes patient outcomes.

To examine the effects of intensive patient and/or physician diabetes education on patient health outcomes, a controlled trial was conducted in which internal medicine residents and their 532 diabetic patients were randomly assigned to: routine care; patient education; physician education; or both patient and physician education. Patient outcome data were analyzed either by analysis of covariance on post intervention values (2-hour post-prandial plasma glucose [PPG]; body weight [BW]; blood pressure [BP]; or analysis of variance conducted on change values (fasting plasma glucose [FPG] and glycosylated hemoglobin [A1Hgb]). After patient education, significant improvements were observed in FPG, A1Hgb, BW, and systolic and diastolic BP. Physician education resulted in significant decreases in FPG, A1Hgb and BW. The combination of patient plus physician education resulted in the greatest improvements in patients' health outcomes including FPG, A1Hgb, PPG, BW and diastolic BP. Adjusted systolic BPs were not significantly different in the two groups. While these physiologic improvements were statistically and probably clinically significant, hyperglycemia and obesity still persisted. Thus, achieving optimal patient outcomes for a chronic disease like diabetes mellitus may require a greater or more effective use of resources than currently estimated.

Clinical Trials as Topic↗
PubMed1985

Regulation of plasma vasopressin in insulin-dependent diabetes mellitus.

Patients with uncontrolled insulin-dependent diabetes mellitus have elevations in plasma vasopressin that cannot be accounted for totally by recognized osmotic or nonosmotic stimuli. To investigate the possibility that regulation of vasopressin secretion is abnormal in this disease, we characterized the vasopressin response to osmotic and hemodynamic stimuli in five uncomplicated, well-controlled insulin-dependent diabetics, and compared the results with those found in nondiabetic volunteers. During osmotic stimulation with hypertonic saline, plasma vasopressin increased in close linear correlation with plasma osmolality or sodium in both groups. However, in the diabetics, the lines describing the relationships between plasma sodium and vasopressin were shifted significantly to the left of normal, suggesting resetting of the osmostat. This shift was not due to abnormal stimulation by hyperglycemia, because increasing plasma glucose and osmolality by intravenous infusion of hypertonic dextrose produced no increase in plasma vasopressin in diabetics or normals. Tilt tests produced a slightly exaggerated increase in plasma vasopressin in diabetics, but their basal and upright pulse rate, blood pressure, plasma renin activity, norepinephrine, and hematocrit were all normal. The results indicate that in diabetic patients the osmoreceptor for osmotic regulation of vasopressin secretion is reset in such a way that higher plasma vasopressin levels are observed at comparable levels of plasma sodium. The exact cause and consequence of this abnormality remain to be determined.

Blood Pressure↗
PubMed1984

Insulin-responsive cultured foetal-rat hepatocytes. Their preparation and characterization.

An improved non-perfusion method for the preparation of cultured foetal-rat hepatocytes is described. Digestion of the liver with collagenase and deoxyribonuclease I gave yields of 40 X 10(6) hepatocytes/g of liver. The plating efficiency of hepatocytes in medium with 10 microM-cortisol was 50%. Cell morphology and metabolism were maintained through 3 days of monolayer culture, with minimal contamination by haematopoietic cells or fibroblasts. The cultured cells bound and degraded 125I-insulin in a time- and dose-dependent manner. The estimated ED50 for competitive binding at 37 degrees C was 1.1 nM. Curvilinear Scatchard plots were observed, with estimates of 16 500 high-affinity sites (Kd = 813 pM) and 53 000 low-affinity sites (Kd = 23 nM) per cell. The cultured cells demonstrated a glycogenic response to insulin, with an estimated ED50 of 120 pM. The degree of glycogenic response to insulin varied with time in culture: 500% above basal on day 1, 200% on day 2, and only 150% on day 3. Cultured foetal cells also exhibited a time-dependent uptake of 2-aminoisobutyric acid, which, in contrast with previous reports with adult cells, was not stimulated by the presence of 10 nM-insulin. Cultured foetal hepatocytes may provide an interesting model with which to study the relationship between insulin-receptor binding and insulin action.

Amino Acids↗
PubMed1980

Adenylyl cyclase responsiveness to guanyl nucleotides in the developing rat heart.

Guanyl nucleotides are effective activators of rat heart adenylyl cyclase activity from the earliest age studied, 16 fetal days, through adulthood. Both guanosine triphosphate and guanylyl-imidodiphosphate (GMP-PNP) significantly enhance epinephrine-stimulated adenylyl cyclase activity at all fetal and postnatal ages. The dose-response curves for epinephrine alone, GMP-PNP alone, or for the combination of epinephrine and GMP-PNP are similar for the newborn and adult heart preparations. Our results indicate that the epinephrine-guanyl nucleotide-adenylyl cyclase system is "mature" as a functional unit in the rat heart even prior to birth. The rat heart adenylyl cyclase system shows a dramatic increase in responsiveness to epinephrine and to guanyl nucleotides just before birth, a responsiveness which rapidly falls by 3 days of neonatal life. With increasing age, the absolute guanosine triphosphate or GMP-PNP activated rate rises in parallel with the basal rate of adenylyl cyclase activity in the rat heart. Speculation. The activation of adenylyl cyclalse systems by guanyl nucleotides may be a general feature of fetal as well as of adult tissues. This activation by guanyl nucleotides may magnify tissue hormonal responses at some stages of development.

Adenylyl Cyclases↗
PubMed1979

Plasma vasopressin in uncontrolled diabetes mellitus.

Concentrations of the antidiuretic hormone, arginine vasopressin, were measured in 28 patients with severe hyperglycemia to determine if abnormalities in hormonal regulation of water excretion could contribute to the extreme dehydration of uncontrolled diabetes mellitus. Vasopressin levels were markedly elevated in both nonketotic and ketotic patients, indicating that vasopressin deficiency plays no role in the polyuria that accompanies hyperglycemia. Instead, the observed increases in vasopressin represent an ineffective effort to conserve water in the face of an overwhelming solute diuresis caused by the glucosuria. The reasons for such marked elevations in plasma vasopressin in these diabetic patients are multifactorial. Both groups of diabetic patients had evidence of hypovolemia, which was sufficient in magnitude to stimulate vasopressin release. Furthermore, nausea provided an independent stimulus to vasopressin secretion in many patients. Osmotic stimulation might have resulted from the large fraction of unidentified plasma solutes, but this factor alone was not sufficient to explain the markedly increased concentrations of vasopressin. Whether such elevations in vasopressin could have metabolic and/or hemodynamic effects in uncrontrolled diabetes remains to be established.

Adolescent↗
PubMed1979

Hyperamylasemia in diabetic ketoacidosis: sources and significance.

The origins and clinical significance of hyperamylasemia during diabetic ketoacidosis are unclear. We have therefore correlated important clinical and laboratory indices of diabetic ketoacidosis with sequential determinations of serum and urine amylase concentrations, amylase/creatinine clearance ratios, and specific amylase isozyme types. Hyperamylasemia occurred in 79% of our patients with diabetic ketoacidosis, often after admission to the hospital. Among these patients, 48% had pancreatic-type, 36% salivary-type, and 16% mixed-type (pancreatic and salivary) hyperamylasemia. There were no correlations between the presence, degree, or isozyme type of hyperamylasemia and most laboratory or clinical characteristics, including gastrointestinal symptoms. Patients with pancreatic-type hyperamylasemia tended to have higher amylase/creatinine clearance ratios, but it was not possible to unequivocably diagnose acute pancreatitis during diabetic ketoacidosis with current routine clinical or laboratory procedures.

Adult↗
PubMed1976

Development of glucagon sensitivity in neonatal rat liver.

The ontogenesis of the hepatic glucagon-sensitive adenylate cyclase system has been studied in the rat. With a partially purified liver membrane preparation, fetal adenylate cyclase was less responsive to glucagon than the enzyme from neonatal or adult livers. Similar results were obtained in gently prepared liver homogenates, suggesting that destruction of essential components of the fetal liver membrane did not account for the relative unresponsiveness of the adenylate cyclase enzyme to glucagon. Investigation of other factors that might account for diminished fetal hepatic responsiveness to glucagon indicate (a) minimal glucagon degradation by fetal membranes relative to 8-day or adult tissue; and (b) available adenylate cyclase enzyme, as suggested by a 13-fold increase over basal cyclic AMP formation with NaF in fetal liver membranes. These results indicate that neither enhanced glucagon degradation nor adenylate cyclase enzyme deficiency accounts for the relative insensitivity of the fetal hepatic adenylate cyclase system to glucagon. In early neonatal life, hepatic adenylate cyclase responsiveness to glucagon rapidly developed and was maximal 6 days after birth. These changes were closely paralleled by a fivefold increase in glucagon binding and the kinetically determined Vmax for cyclic AMP formation. These observations suggest that (a) fetal hepatic unresponsiveness to glucagon may be explained by a limited number of glucagon receptor sites; (b) during the neonatal period, the development of glucagon binding is expressed primarily as an increase in adenylate cyclase Vmax; (c) the ontogenesis of hepatic responsiveness to glucagon may be important in the resolution of neonatal hypoglycemia.

Adenylyl Cyclases↗