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H Ginsberg

Publications and source records attributed to H Ginsberg.

54 records · Page 3Linked to original sources

Metabolic effects of increased caloric intake in man.

In order to determine if increased caloric intake could be responsible for the insulin resistance and elevated plasma glucose, insulin, and triglyceride levels commonly associated with obesity, hypercaloric diets were fed for 3 wk to eight normal subjects, and the metabolic consequences of this diet were assessed before significant weight gain had occurred. One wk of increased caloric intake led to statistically significant increases in fasting plasma insulin (22 per cent), glucose (5 per cent), and triglyceride (30 per cent) levels, as well as an increased insulin response (20 per cent) to oral glucose. Since the average weight gain during this period was only 1.6 kg, the observed changes appear to be secondary to increased caloric consumption, not obesity. Most of these changes returned toward baseline values during the succeeding 2 wk of increased caloric intake, but statistically significant elevations of fasting plasma glucose (10 per cent), insulin (8 per cent) and cholesterol (15 per cent) levels were still seen at the end of the hypercaloric dietary period. On the other hand, insulin resistance, as estimated by direct measurement of insulin responsiveness, did not change as a result of 3 wk of increased caloric intake. These results indicate that acute increases in caloric intake can lead to elevated plasma glucose, insulin, cholesterol, and triglyceride levels. These changes occurred before significant weight gain had taken place, and raised the possibility that at least some of the abnormalities of carbohydrate and lipid metabolism attributed to obesity may be due to increased caloric intake. However, this conclusion would not seem to apply to the insulin resistance associated with obesity, as 3 wk of increased caloric intake did not produce any change in the responsiveness of these subjects to insulin's action.

Adult↗

Quantification of plasma cholesterol and triglyceride levels in hypercholesterolemic subjects receiving ascorbic acid supplements.

In order to assess the possible effects of ascorbic acid on plasma cholesterol and triglyceride levels and plasma lipoprotein composition, nine hypercholesterolemic subjects were treated with oral ascorbic acid (4 g/day) for 2 months. The data demonstrate: 1) no significant change in plasma cholesterol or triglyceride levels; 2) no significant change in the cholesterol or triglyceride concentrations of the major lipoprotein classes; and 3) the unexpected appearance of extra pre-beta bands on lipoprotein electrophoresis by the end of the ascorbic acid treatment period.

Adult↗

Demonstration of insulin resistance in untreated adult onset diabetic subjects with fasting hyperglycemia.

We have used a continuous intravenous infusion of glucose (6 mg/kg/min), insulin (80 mU/min), epinephrine (6 mug/min), and propranolol (0.08 mg/min) to directly assess insulin resistance in 14 untreated adult onset diabetics with a mean (plus or minus SE) fasting plasma glucose level of 217 plus or minus 17 mg/100 ml. During the infusion endogenous insulin secretion is inhibited and steady-state plasma glucose and insulin levels are achieved after 90 min. Since similar steady-state levels of plasma insulin are achieved in all subjects, the plasma glucose concentration observed during the steady-state period is a measure of an individual's insulin resistance. Under these conditions, the mean (plus or minus SE) steady-state plasma glucose level of the 14 diabetic patients was 350 plus or minus 16 mg/100 ml, while that of 12 normal subjects was 121 plus or minus 4 mg/100 ml. Additional studies were performed in which control subjects and patients with diabetes had their fasting plasma glucose levels acutely raised or lowered to comparable levels before receiving the basic infusion mixture of glucose, insulin, epinephrine, and propranolol. The results of these studies indicated that differences in initial plasma glucose levels could not account for the different glucose responses of the two groups to the basic infusion. Finally, the mean (plus or minus SE) steady-state plasma glucose level of 104 plus or minus 17 mg/100 ml observed during the same basic infusion in five patients with fasting hyperglycemia (mean plus or minus SE, 142 plus or minus 12 mg/100 ml) secondary to chronic pancreatitis suggested that neither chronic hyperglycemia nor hypoinsulinemia per se necessarily lead to insulin resistance. These results demonstrate that marked insulin resistance exists in adult onset diabetics with fasting hyperglycemia. Since previous studies have documented the presence of insulin resistance in patients with chemical diabetes, the possibility exists that insulin resistance may be characteristic of adult onset diabetes mellitus.

Adult↗

Kwashiorkor.

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Anemia↗

Lipoprotein metabolism in nonresponders to increased dietary cholesterol.

We have studied the effect of increased dietary cholesterol on production and degradation of plasma very low density lipoproteins and low density lipoproteins. We studied five unselected normal volunteers who were on weight-maintaining diets consisting of 45% carbohydrate, 40% fat, and 15% protein with a ratio of polyunsaturated to saturated fat of 0.4. Cholesterol content was 150 mg/1000 kcal in Period A and 500 mg/1000 kcal in Period B. Subjects were fed each diet for 4 to 5 weeks. The turnover of apoproteins B in very low density and low density lipoproteins and of triglyceride in very low density lipoproteins were measured during the last 2 weeks of each study period using 131I-labeled very low density lipoproteins and 125I-labeled low density lipoproteins and 2-3H-glycerol, respectively. There was no significant change in plasma total cholesterol or triglycerides or in low density lipoprotein cholesterol levels during the high cholesterol versus the low cholesterol diet. Similarly, high cholesterol intake had no effect on the rate of production or clearance of apo B in very low density and low density lipoproteins or of triglyceride in very low density lipoproteins. These data indicate that the flux of very low density lipoproteins does not change in nonresponders to high cholesterol diets.

Adult↗

Increased catabolism of native and cyclohexanedione-modified low density lipoprotein in subjects with myeloproliferative diseases.

We previously demonstrated reduced levels of low density lipoprotein (LDL) cholesterol in association with increased total fractional catabolic rates (FCR( of LDL apoprotein B (apo B) in individuals with myeloproliferative diseases (MPD). The removal of LDL from plasma and interstitial fluid is mediated via receptor and nonreceptor pathways. We attempted to quantitate LDL catabolism via each of these pathways in subjects with MPD and control subjects. The total FCR of LDL apo B was measured using radiolabeled native LDL. The FCR of radiolabeled cyclohexanedione-modified LDL (CHD-LDL) was used to assess the nonreceptor-mediated catabolism of LDL. Total FCR (mean +/- SD) was elevated in MPD vs controls (0.78 +/- 0.32 vs 0.45 +/- 0.11, p less than 0.01). CHD-LDL FCR was also increased in MPD vs controls (0.62 +/- 0.53 vs 0.23 +/- 0.04, p less than 0.01). Studies of the plasma decay of radiolabeled native and CHD-LDL preparations after their injection into cynomolgus monkeys indicated that CHD-LDL preparations from MPD and controls were removed at the same rates in those primates and that all CHD-LDL preparations were catabolized more slowly than the native LDL preparations. Studies in vitro indicated that CHD modification of LDL significantly reduced the rate of degradation of this lipoprotein by a specific high-affinity receptor pathway in normal human monocyte-derived macrophages and cultured human fibroblasts. We conclude that the catabolism of both native and CHD-LDL apo B is increased in subjects with MPD. If CHD-LDL is a valid tracer of nonreceptor-mediated removal of native LDL in individuals with MPD, our results indicate that the reduced LDL cholesterol concentrations demonstrated in these subjects are associated with increased nonreceptor-mediated catabolism of LDL apo B. At this time, both neoplastic cells and activated monocyte-macrophages appear to be likely sites of these abnormalities.

Aged↗

Rapid heating: critical theoretical assessment of thermal gradients found in hyperthermia treatments.

There is increasing evidence that many hyperthermia failures are closely related to the large variability of temperatures found in the treatment field. These are linked to thermal gradients near the treatment boundary, vascular perfusion differences, localized cooling, and poor distribution of energy deposition in the tissues. One way of reducing the temperature gradients is to replace traditional heating treatments of 30-60 min by a rapid heating technique, in which the treatment time is a few seconds combined with higher treatment temperatures. The purpose of this paper is to model potential advantages of using various rapid heating protocols, and to compare them with traditional treatments. Theoretical models (in agreement with clinical treatments) suggest that traditional hyperthermia treatments often do not produce the necessary temperature homogeneity needed to kill the last malignant cells in the tumour due to cooler regions in the field. The simulations presented in this paper suggest that much shorter treatment times (1-10 s) should give significant improvements in the treatment field for both the temperature homogeneity and equivalent thermal doses.

Hyperthermia, Induced↗