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Biomedical subjects

L D Katz

Publications and source records attributed to L D Katz.

31 records · Page 2Linked to original sources
PubMed1992

Increased rate of gluconeogenesis in type II diabetes mellitus. A 13C nuclear magnetic resonance study.

UNLABELLED: To quantitate hepatic glycogenolysis, liver glycogen concentration was measured with 13C nuclear magnetic resonance spectroscopy in seven type II diabetic and five control subjects during 23 h of fasting. Net hepatic glycogenolysis was calculated by multiplying the rate of glycogen breakdown by the liver volume, determined from magnetic resonance images. Gluconeogenesis was calculated by subtracting the rate of hepatic glycogenolysis from the whole body glucose production rate, measured using [6-3H]glucose. Liver glycogen concentration 4 h after a meal was lower in the diabetics than in the controls; 131 +/- 20 versus 282 +/- 60 mmol/liter liver (P < 0.05). Net hepatic glycogenolysis was decreased in the diabetics, 1.3 +/- 0.2 as compared to 2.8 +/- 0.7 mumol/(kg body wt x min) in the controls (P < 0.05). Whole body glucose production was increased in the diabetics as compared to the controls, 11.1 +/- 0.6 versus 8.9 +/- 0.5 mumol/(kg body wt x min) (P < 0.05). Gluconeogenesis was consequently increased in the diabetics, 9.8 +/- 0.7 as compared to 6.1 +/- 0.5 mumol/(kg body wt x min) in the controls (P < 0.01), and accounted for 88 +/- 2% of total glucose production as compared with 70 +/- 6% in the controls (P < 0.05). IN CONCLUSION: increased gluconeogenesis is responsible for the increased whole body glucose production in type II diabetes mellitus after an overnight fast.

Aged↗
PubMed1991

Quantitation of hepatic glycogenolysis and gluconeogenesis in fasting humans with 13C NMR.

The rate of net hepatic glycogenolysis was assessed in humans by serially measuring hepatic glycogen concentration at 3- to 12-hour intervals during a 68-hour fast with 13C nuclear magnetic resonance spectroscopy. The net rate of gluconeogenesis was calculated by subtracting the rate of net hepatic glycogenolysis from the rate of glucose production in the whole body measured with tritiated glucose. Gluconeogenesis accounted for 64 +/- 5% (mean +/- standard error of the mean) of total glucose production during the first 22 hours of fasting. In the subsequent 14-hour and 18-hour periods of the fast, gluconeogenesis accounted for 82 +/- 5% and 96 +/- 1% of total glucose production, respectively. These data show that gluconeogenesis accounts for a substantial fraction of total glucose production even during the first 22 hours of a fast in humans.

Adult↗
PubMed1990

Case report 571: Radiation-induced growth abnormalities.

A case of a 23-year-old man with deformities of the spine and hip is presented, demonstrating the bizarre long term effects of radiation on developing bone. The spectrum of radiation-induced growth abnormalities is reviewed. Multiple variables, including age of the patient, the quantity of radiation delivered, and the site of delivery, all effect the eventual radiographic appearance.

Adult↗
PubMed1990

Influence of combined intravenous and oral glucose administration on splanchnic glucose uptake in man.

The influence of intravenous plus oral glucose administration on splanchnic glucose handling was examined in healthy young individuals by combining the hepatic vein catheterization technique with the double glucose tracer method. After 1 h of steady state hyperglycaemia (11.7 mM) induced by intravenous glucose alone (hyperglycaemic clamp technique), subjects ingested 89 +/- 1 g of glucose, and the hyperglycaemic plateau was maintained for the subsequent 4 h by adjusting the exogenous glucose infusion rate. Over the 4-h absorptive period, only 51 +/- 4 g of oral glucose (i.e. 58 +/- 4% of the ingested load) appeared in the systemic circulation, while 193 +/- 15 g (1.072 +/- 0.83 mol) of glucose had to be infused exogenously to sustain the hyperglycaemia. Endogenous glucose production was suppressed by over 60%. Net splanchnic glucose balance switched from a positive value (i.e. net uptake) of 5.06 +/- 2.56 mumol min-1 kg-1 with intravenous glucose alone (0-60 min) to a negative one (i.e. net output) of 12.50 +/- 2.44 mumol min-1 kg-1 during 4 h (60-300 min) of intravenous + oral glucose. The mean rate of splanchnic glucose uptake was estimated to be 6.39 +/- 4.67 mumol min-1 kg-1 with intravenous glucose alone, and 8.83 +/- 4.28 mumol min-1 kg-1 with intravenous + oral glucose. In either case, the large majority (80-90%) of the glucose appearing in the systemic circulation was disposed of by extrasplanchnic tissues. These results indicate that pre-existing hyperglycaemia and/or hyperinsulinaemia inhibit gastrointestinal glucose absorption, and that oral glucose administration does not result in a major redistribution of intravenous glucose between splanchnic and extrasplanchnic tissues.

Administration, Oral↗
PubMed1988

The disposal of an oral glucose load in patients with non-insulin-dependent diabetes.

Following glucose ingestion, tissue glucose uptake is enhanced and endogenous glucose production is inhibited, thus contributing to the maintenance of normal glucose tolerance. To examine whether these responses are disturbed in diabetes, glucose kinetics after oral glucose administration were studied in 12 non-insulin-dependent diabetic and 10 age- and weight-matched control subjects. A double tracer approach was used, whereby the endogenous glucose pool was labeled with 3-3H-glucose and the oral load with 1-14C-glucose. The two glucose tracers were separated in plasma by a two-step chromatographic procedure, and the two sets of isotopic data were analyzed according to a two-compartment model for the glucose system. Basally, glucose production was slightly higher in diabetics than in controls (2.51 +/- 0.24 v 2.28 +/- 0.11 mg/kg.min, NS) even though the former had higher plasma glucose (189 +/- 19 v 93 +/- 2 mg/dL, P less than .001) and insulin (23 +/- 4 v 12 +/- 1 microU/mL, P less than .05) concentrations. Following the ingestion of 1 g/kg of glucose, oral glucose appeared in the peripheral circulation in similar time-course and amount in the two groups (75 +/- 2% of the load over 3.5 hours in the diabetics v 76 +/- 3% in controls). Endogenous glucose production was promptly inhibited in diabetic and normal subjects alike, but the mean residual hepatic glucose production after glucose ingestion was significantly greater in the diabetic group (17 +/- 2 v 10 +/- 3 g/3.5 h, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

In vivo glucose metabolism in the awake rat: tracer and insulin clamp studies.

The goals of this study were twofold: (1) to determine the in vivo dose-response relationship in the conscious, unstressed rat between the plasma insulin concentration and total body glucose uptake, and between plasma insulin and suppression of endogenous glucose production; and (2) to develop a physiologic compartmental model to describe the kinetics of plasma glucose in the rat in the basal state. In order to perform repeat insulin clamp studies in the same rat, chronic catheters were implanted in the aortic arch (via the carotid artery) and in the cardiac atrium (via the jugular vein), exteriorized, and fixed to the back of the skull with a dental cement cap. Insulin was infused at rates of 1.2, 2.4, 4.8, 12, and 24 mU/min.kg, and the plasma glucose was held constant at the basal level by a variable glucose infusion (euglycemic insulin clamp). The resulting steady-state plasma insulin concentrations ranged from 40 to 1,300 microU/mL. The dose-response curve for glucose uptake was sigmoidal in shape: in the basal state, total glucose utilization averaged 6.8 mg/min.kg at an insulin concentration of 9 microU/mL, half-maximal glucose uptake (18.3 mg/kg.min) occurred at a plasma insulin concentration between 70 and 80 microU/mL, and maximal uptake (36.6 mg/kg.min) was seen at an insulin level in excess of 100 microU/mL. Residual endogenous glucose production was evaluated by a prime-continuous infusion of (3-3H)-glucose. The dose-response curve for suppression of endogenous glucose output also was sigmoidal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effect of epinephrine on renal potassium excretion in the isolated perfused rat kidney.

The effects of beta-agonists (epinephrine, isoproterenol, and ITP) and beta-antagonists (propranolol, metoprolol, and butoxamine) on renal potassium excretion were examined using the isolated perfused rat kidney preparation. Following 30 min of control perfusion, one of the above beta-adrenergic agonists or antagonists was added to the perfusion medium. Following epinephrine, a combined beta 1- and beta 2-agonist, urinary potassium excretion (UKV; 0.55 +/- 0.55 vs. 0.36 +/- 0.04 mueq/min, P less than 0.001) and fractional excretion of potassium (FEK; 24.6 +/- 2.4 vs. 18.2 +/- 2.0%, P less than 0.001) both decreased. When isoproterenol, a nonspecific beta-agonist, was added to the perfusate, UKV (0.49 +/- 0.10 vs. 0.27 +/- 0.04 mueq/min, P less than 0.02) and FEK (29.0 +/- 5.2 vs. 16.3 +/- 2.9%, P less than 0.01) again decreased. ITP, a specific beta 1-agonist also caused a decrease in UKV (0.60 +/- 0.13 vs. 0.39 +/- 0.04 mueq/min, P less than 0.02) and FEK (30.2 +/- 5.1 vs. 17.8 +/- 2.8%, P less than 0.02). In contrast, when propranolol, a nonspecific beta-antagonist, was added to the perfusate, the opposite effects on renal potassium handling were observed. UKV (0.45 +/- 0.05 vs. 0.70 +/- 0.07 mueq/min, P less than 0.001) and FEK (23.0 +/- 2.1 vs. 42.5 +/- 3.1%, P less than 0.001) both increased. Metoprolol (50 ng/ml), a specific beta 1-antagonist, increased UKV (0.56 +/- 0.10 vs. 0.68 +/- 0.15 mueq/min, P less than 0.02) and FEK (31.0 +/- 3.8 vs. 48.0 +/- 7.1%, P less than 0.02). A similar effect was observed when a higher dose of metoprolol (200 ng/ml) was employed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Splanchnic and peripheral disposal of oral glucose in man.

Oral glucose (92 g) was administered to 22 healthy, young volunteers undergoing hepatic vein catheterization, and net splanchnic glucose output (SGO) was measured during the basal period and for 4 h after glucose ingestion. In the basal state, SGO averaged 1.90 +/- 0.11 mg/min X kg. After glucose, SGO rose to a peak value of 6.65 +/- 0.83 mg/min X kg at 30 min and returned to baseline by 3 h. Total SGO over 4 h was 69 +/- 4 g; assuming complete absorption of the load, this amount represented 75% of the oral glucose. In a subgroup of six subjects, leg glucose uptake was simultaneously quantitated by femoral vein catheterization and leg blood flow measurement. In the postabsorptive state, glucose uptake by one leg was 24 +/- 8 mg/min and increased to a mean value of 76 +/- 7 mg/min during the 4 h after glucose ingestion. Overall, 18 +/- 2 g/4 h of glucose were taken up by one leg, which extrapolates to a total body muscle uptake of 65 +/- 4 g over 4 h. We conclude that in normal man, well over 2/3 of an oral glucose load escapes splanchnic removal, and that the peripheral tissues quantitatively play the dominant role in glucose disposal.

Adult↗
PubMed1979

Volvulus of the transverse colon: report of case and review of the literature.

A case of transverse colon volvulus is reported, bringing the total number of collected cases in the English language medical literature to 45. Although this type of volvulus is rare, a definite pattern can be appreciated. Patients tend to be young, female, and give a history of chronic or recurrent difficulty in having bowel movements. A triad of underlying factors predisposes to the development of the volvulus: a distal impediment (either organic or functional) to the evacuation of the bowel, a redundant bowel and mesocolon and a fixed point around which the bowel can twist. The best treatment is resection with either anastomosis or exteriorization, depending on bowel viability.

Adolescent↗
PubMed1979

A method of palliation for obstructive carcinoma of the rectum.

The use of the resectoscope has several advantages in treating the patient with inoperable obstructive carcinoma of the rectum, particularly when compared with fulguration. It is immediate in its results, as often testified to by the sudden outpouring of blockaded feces. It is also safer in allowing greater amounts of tissue to be resected with less depth of tissue injury by the electrical output. It does, however, require the skills of someone able to handle the instrument, and the procedure should be a joint effort by the surgeon and urologist. The use of the urologic resectoscope should prove to be a useful addition in the surgeon's armamentarium in a selected number of patients.

Adenocarcinoma, Mucinous↗