Search PubMed⌕ Search

Biomedical subjects

C N Sadur

Publications and source records attributed to C N Sadur.

12 recordsLinked to original sources
PubMed1999

Diabetes management in a health maintenance organization. Efficacy of care management using cluster visits.

OBJECTIVE: To evaluate the effectiveness of a cluster visit model led by a diabetes nurse educator for delivering outpatient care management to adult patients with poorly controlled diabetes. RESEARCH DESIGN AND METHODS: This study involved a randomized controlled trial among patients of Kaiser Permanente's Pleasanton, CA, center who were aged 16-75 years and had either poor glycemic control (HbA1c > 8.5%) or no HbA1c test performed during the previous year. Intervention subjects received multidisciplinary outpatient diabetes care management delivered by a diabetes nurse educator, a psychologist, a nutritionist, and a pharmacist in cluster visit settings of 10-18 patients/month for 6 months. Outcomes included change (from baseline) in HbA1c levels; self-reported changes in self-care practices, self-efficacy, and satisfaction; and utilization of inpatient and outpatient health care. RESULTS: After the intervention, HbA1c levels declined by 1.3% in the intervention subjects versus 0.2% in the control subjects (P < 0.0001). Several self-care practices and several measures of self-efficacy improved significantly in the intervention group. Satisfaction with the program was high. Both hospital (P = 0.04) and outpatient (P < 0.01) utilization were significantly lower for intervention subjects after the program. CONCLUSIONS: A 6-month cluster visit group model of care for adults with diabetes improved glycemic control, self-efficacy, and patient satisfaction and resulted in a reduction in health care utilization after the program.

Adolescent↗
PubMed1995

Glycohemoglobin levels relate to the response of adipose tissue lipoprotein lipase to insulin/glucose in obese non-insulin-dependent diabetes mellitus.

Adipose tissue lipoprotein lipase (ATLPL) is responsible for the provision of lipoprotein-derived fatty acids to adipocytes for storage as triglycerides. Fasting ATLPL has been shown to be decreased in non-insulin-dependent diabetes mellitus (NIDDM), an insulin-resistant state. Medically uncomplicated obesity, another state of relative insulin resistance, is associated with decreased stimulation of the enzyme in response to metabolic stimuli. It was therefore hypothesized that the increased insulin resistance of NIDDM would result in an even greater defect in the response of ATLPL to insulin/glucose. Gluteal adipose tissue biopsies were performed in 13 premenopausal obese women with NIDDM, before and after 6 hours of intravenous insulin and glucose. Metabolic data from these studies were then compared with those obtained from 26 nondiabetic obese women of similar age, weight, and fasting insulin concentration (obese controls [OBC]). As expected, fasting gluteal ATLPL activity was lower in the NIDDM group than in OBC (3.7 +/- 0.9 v 11.1 +/- 1.6 nmol free fatty acids [FFA]/min/10(6) cells, P = .0003). The change in ATLPL activity (delta ATLPL) in response to a 6-hour insulin/glucose infusion was not statistically different between the two groups (2.2 +/- 1.1 v 4.7 +/- 1.2, P = .114). However, in NIDDM subjects there was a strong positive relationship between delta ATLPL and glycohemoglobin (GHb) level (r = .883, P = .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1992

Cholelithiasis in patients treated with a very-low-calorie diet.

One hundred seventy-nine obese patients (mean body mass index = 36.3) were retrospectively evaluated for the development of cholelithiasis associated with the use of a 2530-kJ/d (605-kcal) very-low-calorie diet (VLCD). Nine percent of patients had preexisting gallstones and 11% of patients developed gallstones either during or within 6 mo of completing the diet. Six percent had subsequent cholecystectomy. Ursodeoxycholic acid administered to one patient resulted in spontaneous stone dissolution whereas spontaneous dissolution occurred in three patients. Surveys of patients at three other programs using the same diet yielded similar incidence of gallstones. We conclude that rapid weight loss associated with the use of VLCD is associated with a significant incidence of gallstone formation. VLCD should be physician supervised because resolution of cholelithiasis spontaneously, with stone passage, or dissolution with ursodeoxycholic acid therapy may reduce the need for cholecystectomy.

Cholecystectomy↗
PubMed1992

Body composition and weight maintenance with a very-low-calorie diet for the treatment of moderate obesity.

We report body composition in 11 moderately obese patients (mean BMI less than 30) treated for 8 wk with a 2530-kJ/d (605-Kcal) diet. Mean weight loss was 9.4 kg. Fat-free mass (FFM) loss of 2.3 kg was 23% of total weight loss and essentially equal to loss of total body water (2.5 L). Body composition was measured by the Futrex-5000 near-infrared technique. We conclude there is no excess loss of FFM in moderately obese patients treated with MNP 70/70, a 70-g protein, 70-g carbohydrate dietary supplement for 8 wk.

Body Composition↗
PubMed1992

Repeated use of the very-low-calorie diet in a structured multidisciplinary weight-management program.

Forty-eight obese patients (mean body mass index = 36.4) were retreated with a very-low-calorie diet (VLCD) at a mean of 104-wk after first VLCD. Mean weight regain was 23 kg or 86% regain of initial loss. Retreatment with VLCD required weekly physician monitoring and indepth psychotherapy group attendance. Five patients (10%) lost an average of 4.55 kg and withdrew within the first 4 wk (group AO. Thirteen patients (27%) lost 13.8 kg over 11.5 wk, an average weight loss of 1.2 kg/wk and enrolled in maintenance (group B). Thirty patients (63%) lost 10.2 kg over 20 wk, an average weight loss of 0.5 kg/wk and did not enroll in the maintenance program (group C). Although weight loss occurs in patients retreated with the VLCD, adherence to the VLCD and commitment to the maintenance program are not optimal.

Adult↗
PubMed1990

Cushing's syndrome in pregnancy.

Fertility and childbearing rarely occur in Cushing's syndrome because amenorrhea, oligomenorrhea, infertility, and abortions characterize the disease. Currently, a total of 53 cases of Cushing's syndrome and pregnancy have been reported. When Cushing's syndrome occurs during pregnancy, approximately 56 per cent of the cases are associated with adrenal cortical adenoma or carcinoma. Excluding Cushing's disease, nearly 21 percent of the cases are caused by adrenal carcinoma. The maternal catabolic state of glucocorticoid excess contributes to poor fetal outcome with many of the cases complicated by either fetal wastage or prematurity. However, congenital malformations are not seen more frequently than in normal pregnancy. Pregnancy may or may not influence Cushing's syndrome, but Cushing's syndrome definitely complicates pregnancy.

Adult↗
PubMed1988

Deficiency of the insulin, glucose-mediated decrease in serum triglycerides in normolipidemic obese subjects.

The effects of a 6-h insulin, glucose infusion on lipid metabolism were compared in 29 normolipidemic obese and 20 control subjects. Alterations in serum triglycerides (TG), cholesterol, and high-density lipoprotein (HDL) cholesterol were similar within groups when either 40 or 120 mU/m2 per min of regular insulin were infused. Although changes in the HDL cholesterol responses to the insulin, glucose infusions were also similar in obese and control subjects, TG fell more in insulin, glucose-infused controls (35 +/- 4 mg/dl, means +/- s.e.m.) than obese subjects (23 +/- 3) (P less than 0.001). The rate and magnitude of the insulin, glucose-mediated fall in free fatty acids, however, were not different between the two groups. This diminished responsiveness of TG to an insulin, glucose infusion in normotriglyceridemic obese subjects is another manifestation of the insulin resistance of obesity.

Adult↗
PubMed1984

Fat feeding decreases insulin responsiveness of adipose tissue lipoprotein lipase.

The acute effect of fat feeding on the insulin-mediated stimulatory response of adipose tissue lipoprotein lipase (ATLPL) was examined in normal-weight subjects. After two days of isocaloric-formula feeding, subjects were divided into the following four groups: intravenous (IV) saline alone (sal) (n = 5), IV saline and 67 g of oral corn oil ingested at the outset of the infusion (sal/fat) (n = 5), IV insulin (40 mU/m2/min) and glucose to maintain euglycemia (ins/glu) (n = 9), and IV insulin and glucose and oral corn oil (ins/glu/fat) (n = 8). Triglycerides fell less in the ins/glu/fat group than in the ins/glu group (0 +/- 8% v 35 +/- 5%, means +/- SEM, at three hours, P less than 0.01; 15 +/- 8% v 43 +/- 6% at six hours, P less than 0.02). ATLPL in the sal and sal/fat groups did not change during the six-hour period. When the responsiveness of ATLPL was compared between ins/glu/fat subjects and ins/glu subjects, decreases were seen at both three and six hours (-0.3 +/- 3.0 v 15.1 +/- 5.4 nEq/g/min, P less than 0.05; 6.7 +/- 2.7 v 27.9 +/- 3.9 nEq/g/min, P less than 0.001). The glucose infusion rates needed to maintain euglycemia were also decreased by fat feeding, 229 +/- 18 v 287 +/- 20 mg/m2/min (P less than 0.05). Thus, fat feeding with insulin and glucose infusions diminishes the insulin responsiveness of ATLPL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1984

Insulin responsiveness of adipose tissue lipoprotein lipase is delayed but preserved in obesity.

Because increases in adipose tissue lipoprotein lipase (ATLPL) may be important in the pathogenesis of obesity, the response of ATLPL to insulin during maintenance of euglycemia was examined in 22 obese and 8 normal weight subjects. Basal levels of ATLPL per g fat tissue for the obese and control groups were 18.7 +/- 2.0 (+/- SEM) and 9.6 +/- 2.7 neq/g X min, respectively. Insulin and glucose infusion rapidly produced antilipolysis in both groups, as evidenced by large falls in FFA by 20 min. When the responses of ATLPL in absolute change from basal were compared between the obese and control groups, no significant differences were found. However, because of the higher baseline ATLPL values in the obese subjects, the percent change in ATLPL from basal was significantly blunted at the 80 (P = 0.02), 180 (P less than 0.05), and 360 (P = 0.005) min timepoints compared to those in the normal subjects. By 3 h into the infusion, the control group had a significant rise in ATLPL above the basal level (4.2 +/- 1.3 ngq/g X min; P = 0.01), whereas the obese group did not (2.3 +/- 1.9 neq/g X min; P = NS). However, by 6 h, the ATLPL per g response above baseline was significantly increased in both normal (19.2 +/- 6.5 neq/g X min; P = 0.01) and obese subjects (9.8 +/- 2.3; P less than 0.001). Because adipose cell size was greater in obese subjects, data were also expressed per 10(6) cells. Basal ATLPL per 10(6) cells [11.8 +/- 1.7 neq/10(6) cells X min (obese); 3.4 +/- 0.9 neq/10(6) cells X min (normal)] was a function of cell size (rs = 0.713; P less than 0.001), body mass index (rs = 0.565; P less than 0.005), and basal insulin levels (rs = 0.434; P less than 0.05). As with the ATLPL per g response, the increases in ATLPL per 10(6) cells above basal were significant at both the 3 and 6 h marks for the normal subjects, but only at the 6 h timepoint for the obese group. Both steady state insulin levels [342 +/- 24 microU/ml (obese); 251 +/- 27 microU/ml (normal)] and the glucose infusion rates needed to maintain euglycemia [319 +/- 23 mg/m2 X min (obese); 312 +/- 33 mg/m2 X min (normal)] did not correlate with changes in ATLPL. Thus, insulin responsiveness of ATLPL in obese subjects was delayed but preserved. This phenomenon may be important in maintenance of the obese state.

Adipose Tissue↗
PubMed1982

Insulin stimulation of adipose tissue lipoprotein lipase. Use of the euglycemic clamp technique.

The role of insulin in the regulation of adipose tissue lipoprotein lipase activity in humans was investigated in 11 normal subjects and compared with the effects of 0.9% saline infusions in five control subjects. After a basal adipose tissue biopsy for lipoprotein lipase activity, insulin was rapidly infused to achieve and maintain serum levels of approximately 70 microunits/ml while plasma glucose was kept at basal concentrations. Free fatty acids in serum fell to 27 +/- 3% of basal by 20 min (t = 5.19, P less than 0.001) and triglycerides decreased to 77 +/- 3% of basal by 80 min (t = 3.76, P less than 0.01). Adipose tissue lipoprotein lipase activity failed to increase significantly above that measured in controls by the first 3 h of the study. By 6 h of the infusion a stimulatory effect of insulin on adipose tissue lipoprotein lipase was found (t = 3.94, P less than 0.01). There was no relationship between the amount of glucose infused and the insulin effect on the enzyme. The increase in adipose tissue lipoprotein lipase activity at 6 h, however, was inversely related to the basal lipase activity (r = -0.690, P less than 0.02). Thus, insulin appears to stimulate adipose tissue lipoprotein lipase activity in humans. This effect of insulin is delayed when compared with antilipolysis and the fall in plasma triglyceride. The inverse relationship between insulin-stimulated adipose tissue lipoprotein lipase activity and basal enzyme activity suggests that adipose tissue itself is the main regulator of the lipase response to insulin.

Adipose Tissue↗
PubMedDate not supplied

Insulin-mediated increases in the HDL cholesterol/cholesterol ratio in humans.

The role of insulin in the regulation of lipoprotein cholesterol distribution was studied in 18 human volunteers who were of normal weight, normolipemic, and glucose-tolerant. We used the euglycemic clamp technique and made comparisons with six saline-infused controls. While total cholesterol and low density lipoprotein cholesterol levels fell similarly by 6 hours in both groups (p = NS), there was a greater decrease in triglyceride levels (p less than 0.02) but less decrease in high density lipoprotein cholesterol levels (p less than 0.02) in the insulin-infused group. These changes resulted in both a higher high density lipoprotein cholesterol/total cholesterol ratio (p = 0.01) and a higher high density lipoprotein cholesterol/low density cholesterol ratio (p = 0.02) in the insulin-infused group. The timing of this effect of insulin implies a mechanism unrelated to high density lipoprotein turnover. Thus, insulin infusion during euglycemia appears to alter cholesterol distribution favorably in normal subjects.

Adult↗