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Biomedical subjects

G Steiner

Publications and source records attributed to G Steiner.

At least 289 records · Page 16Linked to original sources
PubMed1978

Plasma high-density lipoproteins and ischemic heart disease: studies in a large kindred with familial hypercholesterolemia.

The expression of ischemic heart disease was studied in a large kindred with familial hypercholesterolemia. Tendon xanthomas, multiple generation transmission, and the appearance of bimodality in the distributions of total and low-density lipoprotein cholesterol were found. The segregation ratio was 0.9 in females and 0.43 in males, a difference first apparent during adolescence. The upper quartile of total and low-density lipoprotein cholesterol contained all but two cases of ischemic disease, whereas the lower quartile of high-density lipoprotein cholesterol contained one half of the cases. The ratio of high- to low-density lipoprotein cholesterol (range, 0.06 to 1.6) was less than or equal to 0.20 in each patient with ischemic disease. The association of a low level of high-density lipoprotein cholesterol with ischemic disease persisted after adjustment for differences in other lipids and lipoproteins. A low level of high-density lipoprotein cholesterol, as well as a high level of low-density lipoprotein cholesterol, may influence the development of ischemic heart disease in this disorder.

Adolescent↗
PubMed1978

Hyperlipidemia, atherosclerosis, and diabetes.

At present the two different mechanisms underlying the hypertriglyceridemia of diabetes are reasonably well defined. The rationale of therapy has grown from this knowledge. One form of hyperlipidemia is due to the hyperinsulinemia which results from the patient's resistance to insulin. The approach to treatment aims to overcome the insulin resistance. In most patients this is done by treating their obesity. The other form of hypertriglyceridemia results from insulin deficiency and is treated by bringing the patient's diabetes under control. There is strongly suggestive evidence that hypertriglyceridemia may be associated with a high risk of atherosclerosis. The reason for treating hypertriglyceridemia in general, and in the diabetic in particular, is to reduce this risk. However, it must be conceded that, at the moment, there is no information about the effect of lower triglyceride levels on the incidence of atherosclerosis. Hence much epidemiologic research is needed before our rationale for treatment can move from the realm of hope to the realm of definite proof. In the mean time an attack on this and the other risk factors is the best way we have to attempt to prevent the major complication of diabetes, atherosclerosis.

Arteriosclerosis↗
PubMed1977

Normative standards of plasma cholesterol and triglyceride concentrations in Canadians of working age.

Fasting plasma cholesterol and triglyceride concentrations were determined for 6407 working Canadian adults aged 20 to 69 years in Toronto and Hamilton. Means, medians and 5th and 95th percentiles were ascertained from the data for men, women taking oral contraceptives or estrogen preparations, and women not taking such medication. Mean plasma cholesterol values (mg/dL) ranged in men from 168.3 at ages 20 to 24 years to 211.5 at ages 45 to 49 years, and in women using hormone preparations from 180.3 at ages 20 to 24 years to 224.2 at ages 50 to 54 years; corresponding values in women not using these preparations were 164.9 and 220.6. Plasma triglyceride means (mg/dL) ranged in men from 108.7 at ages 20 to 24 years to 166.7 at ages 40 to 44 years, in women using hormone preparations from 115.4 at ages 20 to 24 years to 145.3 at ages 45 to 59 years, and in women not using these preparations from 77.5 at ages 20 to 24 years to 112.4 at ages 50 to 54 years.

Adult↗
PubMed1977

Studies of glucose turnover and renal function in an unusual case of hereditary fructose intolerance.

Examination of glucose kinetics, pancreatic alpha and beta cell function, plasma lipids, urinary acidification and calcium excretion has been undertaken in a patient with hereditary fructose intolerance. This case was unusual as it was associated with insulin-requiring diabetes, type IV hyperlipemia, hypercalciuria and renal calculi. He also demonstrated the previously described fructose-induced defect of urine acidification. Glucagon and C-peptide assays showed that the pancreatic alpha cells were stimulated by fructose and that the beta cells did not respond to fructose. It is not known whether the latter was due to his diabetes or to the lack of a beta cell response to this sugar. Primed 14C-glucose infusions were used for the first time to study nonsteady state glucose kinetics in man. They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. However, after the administration of sorbitol the plasma glucose concentration decreased because glucose production decreased. After the administration of sorbitol there was no change in the metabolic clearance of glucose. This reflects the lack of a peripheral insulin effect and is consistent with the lack of any measurable C-peptide. Glucose utilization also decreased, but this decrease was less than the decrease in glucose production. Because the metabolic clearance of glucose remained unchanged, it was concluded that the change in glucose utilization was solely due to the decrease in glucose concentration. The absence of C-peptide in the plasma indicated that changes in glucose turnover were not related to any changes in endogenous plasma insulin. Furthermore, the plasma glucagon concentration increased and, hence, changes in this hormone could not account for the decrease in glucose production. Therefore, it was concluded that the sorbitol-induced decline in glucose production was due to a direct effect on hepatic metabolism.

Administration, Oral↗
PubMed1977

Turnover and recycling of glucose in man during prolonged fasting.

The effect of prolonged (3-5 wk) fasting on tracer-determined glucose turnover and of recycling radioactive glucose has been examined. We followed the specific activity of plasma glucose after the simultaneous administration of 1-14C-glucose and 3-3H-glucose. The rate of glucose turnover decreased during prolonged fasting. Recycling of radioactive glucose was estimated by two different techniques: (1) the appearance of 14C in positions 2 to 6 glucose was measured; (2) the difference in the slopes of specific activity decline for 1-14C-glucose and for 3-3H-glucose was calculated. The two methods of estimating the radioactive recycling gave results similar to each other. The amount of glucose recycled did not change during prolonged fasting. However, in view of the decline in glucose production during fasting, the proportion of glucose production which was represented by recycling increased. Based on weight and urinary nitrogen loss an estimate of the glucose production from amino acids and glycerol was obtained. The difference between the rate of glucose production from the contribution of amino acids and glycerol and that estimated by radioisotopic techniques was much larger than the measured rate of recycling. This finding suggests that either a large exchange of 12C with 14C occurred in some glycolytic intermediates or that a hitherto unknown source of carbon for glucose production appeared during prolonged fasting.

Adult↗
PubMed1977

The effects of prolonged fasting on plasma triglyceride kinetics in man.

Studies were undertaken to examine triglyceride turnover in obese humans on isocaloric balanced diets and during prolonged (3-5 wk) fasting. The data were related to plasma concentrations of insulin (IRI), glucagon (IRG), and free fatty acids (FFA) and to blood ketone concentrations. The triglyceride turnover rates were also related to the plasma triglyceride concentration. This relationship was the same in the obese on isocaloric balanced diets as that we have previously observed in lean humans on similar diets. The relationship between triglyceride turnover and concentration changed during prolonged fasting in a way that suggested that triglyceride removal was impaired. This viewpoint is consistent with the known effects of fasting on adipose tissue lipoprotein lipase activity. In another group of fasted obese, refed with a hypocaloric diet, the relationship returned toward normal. In addition to the impaired triglyceride removal, prolonged fasting resulted in a decrease in triglyceride production. This decrease occurred despite an increase in plasma FFA. After 3-5 wk of fasting the IRI was about 50% of the initial value, while the IRG was the same as the initial value. While triglyceride production fell during fasting, the blood ketone concentration rose. Others have seen similar changes in ketones and triglycerides in livers perfused with medium in which the ratio of insulin to glucagon fell. The rate of triglyceride production was not related to body weight. However, regardless of nutritional state, it was positively related to the basal plasma insulin levels. These data indicate that, in man as in animal preparations, insulin may regulate hepatic triglyceride production.

Diet, Reducing↗
PubMed1977

A new method for the fractionation of human plasma high density lipoprotein.

We have devised a new method for the fractionation of human plasma high density lipoprotein (HDL). The HDL was chromatographed on DEAE-agarose columns using a continuous gradient of 0.06--0.15 M NaCl. The elution pattern obtained showed three phases, each with differing peptide composition. Examination of the three subfraction showed that each contained both apoA-I and apo A-II, but in different proportions. Subfraction 1 contained no apo C-II or C-III-1 and only a trace of apo C-III-2, subfraction 2 contained apo C-II and C-III-1 but no C-III-2, while subfraction 3 contained considerable apo C-III-2 with only traces of apo C-II or C-III-1.

Apolipoproteins↗
PubMed1977

Tri-hopsital diabetes education centre: a cost effective, cooperative venture.

Six years ago, three teaching hospitals in Canada's fastest growing metropolitan area decided to pool their resources, share facilities and staff to develop a patient education program for the diabetic and his family that would emphasize preventive aspects of medicine and ambulatory care. The venture has paid off handsomely in terms of well informed, highly motivated patients and more effective utilization of costly hospital facilities.

Ambulatory Care↗
PubMed1976

Fractionation of human low density lipoprotein by column chromatography.

We have devised a method to fractionate low density lipoprotein (LDL) into subspecies by means of column chromatography. DEAE-agarose columns, 2.6 X 60 cm, were loaded with LDL (25-45 mg LDL protein) and eluted with a 0.045-0.13 M NaCl gradient. The LDL eluted over a volume of 900 ml. Specific portions of the eluted LDL, reapplied to a column identical with the original, reelute at about the same point. Altering the NaCl concentration of the elution fluid changed the elution volume. The cholesterol-protein ratio of the LDL subfractions was progressively lower in fractions eluting at higher NaCl concentrations. These results indicate the LDL is not a homogenous lipoprotein species but consists of subfractions which differ in at least charge and cholesterol content.

Apoproteins↗
PubMed1976

Effect of serotonin on brown adipose tissue and on its sympathetic neurons.

Previously we have shown that there are two types of sympathetic neurons in the rat interscapular brown fat-pad: long adrenergic neurons with cell bodies located in the paraspinal ganglia and short adrenergic neurons with cell bodies located within the pad itself. The present studies examine 1) the uptake of [3H]norepinephrine by these neurons, 2) the effect of serotonin on release of the catecholamine, and 3) the metabolic action of serotonin on brown fat. [3H]norepinephrine uptake from the medium in which brown fat slices are incubated is linear with time up to 90 min. This uptake is blocked by both cocaine and imipramine. As these drugs block uptake by sympathetic neurons, the [3H]norepinephrine is probably taken up by neurons and not by some other cell in the pad. Serotonin creatinine sulfate, but not creatinine sulfate, promotes the release of the catecholamine from these neurons. Serotonin also exerts a norepinephrine-like metabolic effect on slices of normal brown fat. It stimulates lipolysis and inhibits lipogenesis. Serotonin has no effect on isolated brown fat cells or on slices of reserpinized tissue. It also does not potentiate the action of norepinephrine on these last two preparations. Therefore serotonin's action on brown fat is mediated by norepinephrine-containing stromal cells. The data suggest that the rat brown fat-pad has sympathetic neurons that can take up norepinephrine and that serotonin exerts its metabolic effect by stimulating the release of norepinephrine from these neurons.

Adipose Tissue, Brown↗
PubMed1976

Defective triglyceride removal in lipemia associated with peritoneal dialysis and haemodialysis.

Plasma lipids were measured in 78 uremic patients receiving either chronic peritoneal dialysis or haemodialysis. Type IV hyperlipemia was found in 60% of patients. The lipid level was not influenced by dietary habits or patient's age. Patients on chronic peritoneal dialysis had a significantly higher and more sustained hyperlipemia than the patients on haemodialysis. Triglyceride turnover studies showed that all patients, regardless of the type of dialysis or lipid level, had impaired triglyceride removal as the cause of this lipemia. This defect in triglyceride metabolism was only partially corrected by increasing the efficiency of the dialysis.

Adult↗
PubMed1975

Inhibition of lipoprotein lipase by uremic plasma, a possible cause of hypertriglyceridemia.

In an attempt to define pathogenesis of the previously described impaired triglyceride (TG) removal in uremia, the effects of the addition of normal and uremic plasma on the activity of lipoprotein lipase (LPL) from rat epididymal adipose tissue were examined. Six uremic patients on chronic dialysis and 13 normals were studied. Adding increments of normal and uremic plasma increased the LPL activity to maximal levels when 0.1 ml of plasma was added. Larger aliquots of uremic plasma produced marked inhibition of LPL activity. This inhibition was not observed with the normal plasma. When increasing amounts of uremic plasma were added to an incubation mixture already maximally activated by 0.1 ml of normal plasma, inhibition of LPL was again observed. This inhibition was still present in uremic plasma which had been dialysed against cold saline. The inhibitor was in the lipoprotein-free (d greater than 1.225) fraction of the plasma. The results indicate that uremic plasma has an LPL inhibitor which is probably a protein and may play a role in the pathogenesis of uremic hypertriglyceridemia.

Adipose Tissue↗