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Biomedical subjects

O Hamberg

Publications and source records attributed to O Hamberg.

At least 19 recordsLinked to original sources
PubMed2001

Reduced mitochondrial adenosine triphosphate synthesis in skeletal muscle in patients with Child-Pugh class B and C cirrhosis.

Patients with cirrhosis of the liver often complain of tiredness and a lack of strength at physical exercise. Other investigators have found that muscle strength, work capacity, and maximal oxygen consumption are reduced in cirrhosis. We hypothesized that mitochondrial maximal rate of ATP synthesis in skeletal muscle may be impaired in these patients. This was tested with (31)P nuclear magnetic resonance spectroscopy in anterior tibial muscle of cirrhotic patients and healthy controls at rest, during exercise, and subsequent recovery. In patients with Child-Pugh class B and C cirrhosis resting PCr/P(i) ratio (8.3 +/- 1.0; n = 7) was lower than in patients with Child-Pugh class A cirrhosis (12.1 +/- 2.1; n = 7) and controls (11. 7 +/- 1.1; n = 6; P =.03), while the resting P(i)/gammaATP ratio was higher in Child-Pugh class B and C patients (0.43, 0.30, and 0.27, respectively; P =.03). Maximal rate of mitochondrial adenosine triphosphate (ATP) synthesis (V(max)) as calculated from the initial rate of phosphocreatine (PCr) recovery after work was lower in Child-Pugh class B and C cirrhosis (0.189 mmol/L/s +/- 0.034) than in both Child-Pugh class A patients (0.402 mmol/L/s +/- 0.103) and controls (0.425 mmol/L/s +/- 0.064; P =.01). V(max) was significantly correlated to intracellular free [Mg(2+)] obtained from the (31)P nuclear magnetic resonance (NMR) spectra (P =.003). Insufficient oxygen delivery did not seem a likely cause of reduced ATP synthesis in the patients. These findings suggest either a decreased number of mitochondria in skeletal muscle of the cirrhotic patient in Child-Pugh class B and C or a defective mitochondrial function that could be related to low intracellular free [Mg(2+)].

Adenosine Triphosphate↗
PubMed2001

Urea synthesis in patients with chronic pancreatitis: relation to glucagon secretion and dietary protein intake.

BACKGROUND & AIMS: Up-regulation of urea synthesis by amino acids and dietary protein intake may be impaired in patients with chronic pancreatitis (CP) due to the reduced glucagon secretion. Conversely, urea synthesis may be increased as a result of the chronic inflammation. The aims of the study were to determine urea synthesis kinetics in CP patients in relation to glucagon secretion (study I) and during an increase in protein intake (study II). METHODS: In study I, urea synthesis rate, calculated as urinary excretion rate corrected for accumulation in total body water and intestinal loss, was measured during infusion of alanine in 7 CP patients and 5 control subjects on spontaneous protein intake. The functional hepatic nitrogen clearance (FHNC), i.e. urea synthesis expressed independent of changes in plasma amino acid concentration, was calculated as the slope of the linear relation between urea synthesis rate and plasma alpha -amino nitrogen concentration. In study II, 6 of the patients of study I had urea synthesis and FHNC determined before and after a period of 14 days of supplementation with a protein-enriched liquid (dietary sequence randomized). RESULTS: Study I: Alanine infusion increased urea synthesis rate by a factor of 10 in the control subjects, and by a factor of 5 in the CP patients (P<0.01). FHNC was 31.9+/-2.4 l/h in the control subjects and 16.5+/-2.0 l/h (P<0.05) in the CP patients. The glucagon response to alanine infusion (AUC) was reduced by 75 % in the CP patients. The reduction in FHNC paralleled the reduced glucagon response (r(2)=0.55, P<0.01). Study II: The spontaneous protein intake was 0.75+/-0.14 g/(kg x day) and increased during the high protein period to 1.77+/-0.12 g/(kg x day). This increased alanine stimulated urea synthesis by a factor of 1.3 (P<0.05), FHNC from 13.5+/-2.6 l/h to 19.4+/-3.1 l/h (P<0.01), and the glucagon response to alanine infusion (AUC) by a factor of 1.8 (P<0.05). CONCLUSIONS: Urea synthesis rate and FHNC are markedly reduced in CP patients. This is associated with, and probably a result of, impaired glucagon secretion, and predicts a lower than normal postprandial hepatic loss of amino nitrogen. An increase in dietary protein intake increases alanine stimulated urea synthesis and FHNC by a mechanism that involves an increase in glucagon. This indicates that the low FHNC during spontaneous protein intake included an adaptation to the low protein intake, effectuated by a further decrease in glucagon secretion.

Adaptation, Physiological↗
PubMed2000

Effects of budesonide and prednisolone on hepatic kinetics for urea synthesis.

BACKGROUND/AIMS: Glucocorticoids upregulate hepatic urea synthesis and cause protein breakdown to prevail over synthesis, releasing amino acids into the blood stream and increasing the substrate supply for hepatic urea synthesis. Budesonide is a new generation glucocorticoid that may be used for treatment of inflammatory diseases, e.g. Crohn's disease and autoimmune hepatitis. Due to its extensive first-pass metabolism in the liver, it has a potential adverse effect profile superior to that of prednisolone. Little attention has been directed towards differences in nitrogen catabolic properties between budesonide and prednisolone. METHODS: Eight normal male subjects (age 20-44 years; BMI 21.6-28.2 kg/m2) were randomly studied 3 times: 1) At baseline, 2) after 6 days of prednisolone (50 mg/day), and 3) after 6 days of budesonide (9 mg/ day). We measured urea nitrogen synthesis rates (UNSR) and blood alpha-amino-nitrogen (N) levels before, during, and after a 3-h constant infusion of alanine (2 mmol/(kg BW x h)). UNSR was estimated hourly as urinary excretion corrected for gut hydrolysis and accumulation in body water. The slope of the linear relationship between UNSR and amino-N concentration represents the hepatic kinetics of conversion of amino- to urea-N, and is denoted the functional hepatic nitrogen clearance (FHNC). RESULTS: Prenisolone, but not budesonide, administration increased basal blood and amino nitrogen concentrations (3.5 +/- 0.1 mmol/l (control) vs 3.8 +/- 0.1 mmol/l (prednisolone) (p<0.05) and 3.6 +/- 0.1 mmol/l (budesonide) (NS). Basal UNSR values were significantly increased following prednisolone (23.3 +/- 6.5 (control) vs 51.2 +/- 6.3 (prednisolone) (p<0.05)), while budesonide had no effect on basal UNSR (33.7 +/- 4.2 (budesonide) (NS)). Prednisolone administration increased FHNC (from 24.6 +/- 4.7 l/h (control) to 47.3 +/- 5.9 l/h (prednisolone) (p<0.05). Budesonide administration did not significantly increase FHNC (33.7 +/- 4.2 l/h (budesonide), (vs control; p=0.12, vs prednisolone: p<0.05)). CONCLUSIONS: Prednisolone administration led to increased levels of amino acids in blood and loss of N as urea, the latter in part due to a specific hepatic mechanism as shown by the increased FHNC. Budesonide led to unaltered levels of amino acids in blood, no changes in loss of N as urea, and unaltered hepatic kinetics for urea synthesis. Thus, oral budesonide administration had very limited effects on the hepatic contribution to nitrogen homeostasis and metabolism via urea synthesis, making treatment with budesonide superior to that of conventional glucocorticoids in this respect.

Adult↗
PubMed1999

Effect of a new starch-free bread on metabolic control in NIDDM patients.

BACKGROUND AND AIM: The aim of the study was to evaluate the effect on blood glucose levels in non-insulin-dependent diabetics (NIDDM) of reduction of the carbohydrate content through the use of a new, almost starch-free type of bread (SF-bread). We only substituted the bread in the breakfast meal. METHODS AND RESULTS: The study consisted of two parts: 1) a two-day randomized study of the effect of SF-bread on the morning blood glucose levels of NIDDM patients and 2) an open, crossover trial of three months duration where each patient was given SF- or ordinary bread. Ten patients participated in the first part and eight in the second part of the study. All patients had well established non insulin-dependent diabetes mellitus. In the first part of the study, the area under the curve describing time-dependent changes in blood glucose level after a standard breakfast was significantly lower in patients on SF-bread (182 +/- 154 Units; mean value +/- SD) than in the controls (630 +/- 258 Units; p < 0.00001). Peak blood glucose concentration was 14.8 +/- 2.3 mM on the control day and 11.6 +/- 1.7 mM on the SF-bread day (p < 0.001). In the second part of the study, the diet including SF-bread reduced fasting blood glucose from 13.3 +/- 3.5 mM to 10.2 +/- 2.0 mM (p < 0.006) and the fraction of HbA1c from 0.090 +/- 0.014 to 0.081 +/- 0.015 (p < 0.02). Similar changes were not seen on the ordinary diet. Serum cholesterol levels were significantly reduced by the SF-bread as compared to the ordinary diet (5.8 +/- 0.6 to 5.5 +/- 0.5 mM versus 5.7 +/- 0.8 to 5.8 +/- 0.7 mM; p < 0.05). CONCLUSIONS: Substitution of ordinary bread with starch-free bread at breakfast causes significant improvements in blood glucose levels in NIDDM patients on both a short and long term basis. Possibly secondary to this, a favorable influence on lipid levels was noted.

Aged↗
PubMed1997

[Increased urea synthesis in patients with active inflammatory bowel disease].

Patients with active inflammatory bowel disease are often reported to be in negative nitrogen balance. Therefore, we examined basal and amino acid stimulated urea synthesis in 11 patients with active inflammatory bowel disease and in 10 patients with non-active disease. A primed continuous infusion of an amino acid mixture was given from t = 1 h to t = 5 h; during the first and the last two hours no amino acid infusion was given. Urea nitrogen synthesis rate was quantified independently of changes in blood amino acid concentration by means of the functional hepatic nitrogen clearance, i.e. the linear slope of the regression of urea nitrogen synthesis rate on blood amino acid concentration. Basal and amino acid stimulated urea nitrogen synthesis rate as well as functional hepatic nitrogen clearance were elevated twofold in the patients with active disease. No differences between the two groups were observed as regards basal or stimulated plasma glucagon, cortisol, catecholamines and serum levels of interleukin-1 alpha, interleukin-1 beta, tumor necrosis factor-alpha and interleukin-6. The results show that liver function related to conversion of amino-nitrogen to urea is increased and may contribute to the less efficient nitrogen economy in patients with active inflammatory bowel disease.

Adult↗
PubMed1997

Regulation of urea synthesis by diet protein and carbohydrate in normal man and in patients with cirrhosis. Relationship to glucagon and insulin.

Diet protein increases whereas carbohydrates decrease urea synthesis. Traditionally, these effects have been explained by changes in substrate supply. Diet protein intake increases whereas carbohydrate decreases blood amino acid concentration. However, glucose also decreases urea synthesis by a hepatic mechanism independent of the decrease in blood amino acid concentration. Whether this is due to an effect of glucose in itself, or whether the fall in glucagon or the rise in insulin is responsible, was not known. This survey deals with the effect of an increase in diet protein intake and of the separate effects of glucose, glucagon and insulin on functional hepatic nitrogen clearance in normal man and in patients with cirrhosis of the liver. The functional hepatic nitrogen clearance is calculated as the slope of the linear regression analysis of alanine-stimulated urea synthesis rate and blood alpha-amino nitrogen concentration, and expresses urea synthesis independent of changes in blood amino acid concentration. In patients with cirrhosis, hepatic nitrogen clearance is reduced in parallel with liver cell mass, despite high glucagon concentration that would normally up-regulate the process. In both healthy subjects and in patients with cirrhosis, an increase in diet protein intake (plus approximately 50 g/day) for 14 days increases hepatic nitrogen clearance by 40%. Thus, in addition to the substrate effect, protein intake increases urea synthesis by an effect in the liver, probably by enzyme formation. What induces this is not clear but high postprandial levels of glucagon may be involved. Although the effect is qualitatively intact in the patients, the response relative to the increase in protein intake is reduced by two-thirds. The effect may be important to control blood amino acid concentration during a high protein diet and may partly explain why patients with cirrhosis usually tolerates protein hyperalimentation without developing hepatic encephalopathy. It is shown that the reduction of hepatic nitrogen clearance by glucose depends on hyperglycaemia, and is accomplished by the additive effects of a direct hormone-independent action of glucose, and indirectly via suppression of glucagon. Insulin is not a direct controller of hepatic nitrogen clearance, but is still considered an important regulator of urea synthesis by its reducing effects on blood amino acid concentration. High experimental glucagon levels overrule the normal suppressive effect of glucose. In contrast, it is shown that the sugar-alcohol xylitol normalises the glucagon induced increase in hepatic nitrogen clearance. During normal glucagon levels xylitol exerts only a very little decrease in hepatic nitrogen clearance. In patients with cirrhosis, glucose does not down-regulate hepatic nitrogen clearance. However, when the spontaneous high glucagon levels are normalised by somatostatin, glucose decreases hepatic nitrogen clearance. This shows that the direct hormone-independent effect of glucose is intact. These findings indicate that the high glucagon levels during spontaneous hormone responses overrule the suppressive effect of glucose. Incomplete glucose suppression of glucagon secretion during alanine infusion contributes to the high glucagon levels. The removal of the high glucagon levels decreases hepatic nitrogen clearance in itself. Thus, the hyperglucagonaemia may be a compensatory mechanism by which the cirrhotic liver to some extent reestablishes its capacity to produce urea. The consequence is the defective down-regulation of hepatic nitrogen clearance by glucose. The reduction in urea synthesis by glucose, i.e. its nitrogen sparing effect, is accomplished by two different mechanisms: A hepatic component (reduction of the hepatic nitrogen clearance) and a peripheral component (reduced substrate availability mediated by the insulin response). This is an extension of former thoughts according to which glucose reduces urea synthesis due solely to

Dietary Carbohydrates↗
PubMed1996

Increased hepatic urea synthesis in patients with active inflammatory bowel disease.

BACKGROUND/METHODS: Patients with active inflammatory bowel disease are often reported to be in negative nitrogen balance. Therefore, we examined basal and amino acid stimulated urea synthesis in 11 patients with active inflammatory bowel disease (six with Crohn's disease and five with ulcerative colitis) and in 10 patients with non-active disease (six with Crohn's disease and four with ulcerative colitis). A primed continuous infusion of an amino acid mixture was given from t = 1 h to t = 5 h; during the first and the last 2 h no amino acid infusion was given. Urea nitrogen synthesis rate was calculated in hourly intervals for 7 consecutive hours. Urea nitrogen synthesis rate was quantified independent of changes in blood amino acid concentration by means of the functional hepatic nitrogen clearance, i.e. the linear slope of the regression of urea nitrogen synthesis rate of blood amino acid concentration. RESULTS: Basal urea nitrogen synthesis rate was 24.5 +/- 2.9 mmol/h in the patients with no disease activity and 43.8 +/- 2.2 mmol/h in patients with active disease (p < 0.01). During amino acid infusion urea nitrogen synthesis rate was elevated two-fold in the patients with active disease. Functional hepatic nitrogen clearance was 28.2 +/- 1.5 1/h in patients with no disease activity and 56.1 +/- 4.1 1/h in patients with active disease (p < 0.01). No differences between the two groups were observed as regards basal or stimulated plasma glucagon and cortisol and serum levels of interleukin-1 alpha, interleukin-1 beta, tumor necrosis factor alpha and interleukin-6. CONCLUSIONS: The results show that the liver function related to conversion of amino-nitrogen to urea is increased in patients with active inflammatory bowel disease. No differences among known and possible regulators of urea synthesis were found between the two groups. The accelerated hepatic amino-nitrogen conversion contributes to the less efficient nitrogen economy in patients with active inflammatory bowel disease.

Adolescent↗
PubMed1995

Hormonal regulation of circulating insulin-like growth factor-binding protein-1 phosphorylation status.

Insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) normally circulates as a single, highly phosphorylated species. However, IGFBP-1 phosphorylation status can be altered, such as in pregnancy where non- and lesser phosphorylated isoforms are also present. We have examined how hormonal regulators of circulating IGFBP-1 influence its phosphorylation status and, hence, its ability to modulate IGF activity. In response to insulin-induced hypoglycemia (0.2 U/kg, iv), an increase in the highly phosphorylated isoform was observed after 5 h [16 (range, 11.5-35.5) to 77 (range, 63-250) microgram/L; 4.8-fold increase; P = 0.009], but no non- or lesser phosphorylated variants could be detected. Glucagon (1 mg, sc), increased IGFBP-1 from 27 (range, 13-36.5) to 112 (range, 100.5-129) micrograms/L (4.1-fold increase; P = 0.009) after 90 min despite preceding insulin concentrations of more than 500 pmol/L, but again the IGFBP-1 remained in the highly phosphorylated form. Regulation of IGFBP-1 phosphorylation by sex steroids was studied by comparing women receiving a combined oral contraceptive with women on no medication. Although plasma IGFBP-1 levels were significantly elevated in the treatment group [120 (range, 97.5-237.5) vs. 52 (range, 38-70) micrograms/L; P < 0.004], there was no difference in the form of IGFBP-1 present. The acute effect of somatostatin (500 micrograms/h) on IGFBP-1 phosphorylation status was also studied. Somatostatin only increased the phosphoform characteristic of normal subjects; the appearance of non- or lesser phosphorylated variants was not induced. The effect of rhIGF-I (80 or 120 micrograms, sc) on plasma IGFBP-1 was studied in three subjects with Laron's syndrome. A transient increase in the highly phosphorylated isoform of IGFBP-1 was noted; there was no rise in the non- and lesser phosphorylated isoforms also found in the plasma of Laron's syndrome subjects. These data suggest that only the highly phosphorylated species of IGFBP-1 is under hormonal control; regulation of the non- and lesser phosphorylated variants remains to be determined.

Adult↗
PubMed1994

Effects of insulin and glucose on urea synthesis in normal man, independent of pancreatic hormone secretion.

We investigated the inhibitory effect of insulin and glucose on hepatic amino- to urea-nitrogen conversion independent of endogenous insulin and glucagon secretion. Alanine-stimulated urea synthesis kinetics, as quantified by functional hepatic nitrogen clearance, i.e. the slope of the linear relation between blood alpha-amino nitrogen concentration and urea synthesis rate, were measured four times in each of six healthy volunteers, namely during spontaneous hormone responses, and during hormonal control by somatostatin and maintenance of basal hormone levels and euglycaemia, hyperinsulinaemia (85 +/- 8 mU/l), or hyperglycaemia (8.4 +/- 0.5 mmol/l). Hormonal control and euglycaemia reduced functional hepatic nitrogen clearance (mean +/- SD) by two-thirds (from 32.9 +/- 5.2 l/h to 12.2 +/- 3.4 l/h, p < 0.01). Hyperinsulinaemia did not change this (13.2 +/- 2.8 l/h), whereas hyperglycaemia further reduced functional hepatic nitrogen clearance by 40% to 7.4 +/- 1.3 l/h (p < 0.01). The reduction by hormonal control and euglycaemia is attributable to the abolition of the glucagon response to alanine infusion, as glucagon is known to up-regulate functional hepatic nitrogen clearance. Insulin did not regulate hepatic amino- to urea-nitrogen conversion, implying that the effect of insulin on urea production is due to its effect on blood amino acid supply to the liver. In contrast, glucose in itself reduced hepatic amino nitrogen conversion, independent of the hormonal responses to glucose. This means that the hepatic component of the amino-N-sparing effect of glucose depends on hyperglycaemia but not on hyperinsulinaemia.

Adult↗
PubMed1994

Somatostatin-stimulated insulin-like growth factor binding protein-1 release is abolished by hyperinsulinemia.

It was demonstrated recently that administration of lanreotide and octreotide, two somatostatin octapeptide analogs, increased circulating insulin-like growth factor binding protein 1 (IGFBP-1) levels. The present study demonstrates that native somatostatin 14 shares this ability and that the increase in abolished by concomitant hyperinsulinemia within the physiological range. Five fasting healthy volunteers underwent a hyperinsulinemic as well as a normo-insulinemic (i.e. basal insulinemic) euglycemic clamp lasting 8 h (serum insulin levels remained constant, about 570 vs. 16 pmol/L). Immediately before the clamps, a somatostatin infusion (500 micrograms/h) was started and continued throughout. During normo-insulinemia, IGFBP-1 levels increased slowly from 6.3 +/- 6.2 to 36.1 +/- 14.8 micrograms/L (P < 0.05) reaching maximum after 7 h constant somatostatin infusion, whereas hyperinsulinemia induced a significant decrease from basal levels (from 4.7 +/- 5.4 to 1.1 +/- 1.5 micrograms/L) after 8 h (mean +/- SD, n = 5). These results may indicate hitherto unnoticed interactions of somatostatin and insulin on IGFBP-1 release with possible impact on IGF-I action at the cellular level.

Adult↗
PubMed1994

A rapid method for determination of hepatic amino nitrogen to urea nitrogen conversion ('the Functional Hepatic Nitrogen Clearance').

The Functional Hepatic Nitrogen Clearance (FHNC) is a measure of the functional liver mass as to conversion of amino-N to urea-N. FHNC is the slope of the linear regression of multiple samples (10-20) of urea-N synthesis rates (UNSR) on blood alpha-amino-N concentrations (alpha-AN) during infusion of amino acids. UNSR is measured as urinary urea-N excretion rate corrected for accumulation in total body water (TBW) and loss in gut. A simplified method which estimates FHNC from only two samples of UNSR and alpha-AN was developed. Urine was collected in two hourly intervals: before infusion of alanine, and from 2 to 3 h after start of alanine infusion. Blood-urea-N and alpha-amino-N was measured at the beginning and at the end of each urine sampling interval. TBW was estimated from a nomogram, and gut loss of urea was assigned a fixed value (14%). The two-sample FHNC was calculated as delta UNSR (mmol h-1)/delta mean alpha-AN (mmol l-1). Linear regression analysis of the two-sample estimates of FHNC on the 'true' multiple-sample values of FHNC in an independent population of control and cirrhotic subjects showed the two-sample estimates to be closely related with values of the multiple-sample method, the regression equation being: two-sample FHNC = -0.24 + 0.99 x multiple-sample FHNC, r2 = 0.98. A close relationship was also obtained when cirrhotic patients were considered alone: two-sample FHNC = 0.01 + 0.94 x multiple-sample FHNC, r2 = 0.98.(ABSTRACT TRUNCATED AT 250 WORDS)

Amines↗
PubMed1994

Effects of glucose on hepatic conversion of aminonitrogen to urea in patients with cirrhosis: relationship to glucagon.

Glucose reduces the hepatic conversion of aminonitrogen to urea, quantified by the functional hepatic nitrogen clearance (i.e., the slope of the linear relation between urea synthesis rate and blood alpha-aminonitrogen concentration). This is due to a direct effect of glucose and to inhibition of glucagon. In this study, the effect of glucose on functional hepatic nitrogen clearance was examined during spontaneous hormone responses and during hormonal control by somatostatin. In 7 control subjects (study 1) and 9 patients with cirrhosis (study 2), functional hepatic nitrogen clearance was assessed twice in each subject: during infusion of alanine and during alanine administration superimposed on a continuous glucose infusion (blood glucose, on average = 8.4 mmol/L). In study 3, 6 patients with cirrhosis had functional hepatic nitrogen clearance determined on three occasions: during infusions of alanine and of alanine superimposed on infusion of somatostatin with either euglycemia or hyperglycemia (blood glucose = 8.4 mmol/L). In the control subjects (study 1), functional hepatic nitrogen clearance was 32.5 +/- 1.9 L/hr, and glucose reduced it to 18.4 +/- 0.9 L/hr (p < 0.01). In the cirrhotic patients, functional hepatic nitrogen clearance was only 9.8 +/- 1.3 L/hr (p < 0.01 vs. controls), and glucose did not change it. In the control subjects, glucose reduced the glucagon response to alanine from 204 +/- 36 ng/L to 106 +/- 8 ng/L (p < 0.05). In the cirrhotic patients the mean fasting glucagon level was increased twofold (180 +/- 21 ng/L). The response to alanine increased to 968 +/- 265 ng/L; it was not reduced by glucose. In study 3, somatostatin and hyperglycemia reduced functional hepatic nitrogen clearance from 13.2 +/- 1.5 L/hr to 6.4 +/- 0.7 L/hr (p < 0.01). Somatostatin and euglycemia reduced functional hepatic nitrogen clearance to 9.2 +/- 1.2 L/hr (p < 0.01 vs. alanine and hyperglycemia). The results show that the reduction by glucose of hepatic aminonitrogen conversion is lost in cirrhotic patients. The markedly increased glucagon response to alanine was not suppressed by glucose. Inhibition of the glucagon response by somatostatin reestablished the glucose effect, which was in part due to inhibition of glucagon in itself. Thus hepatic aminonitrogen conversion in cirrhosis depends on increased glucagon levels. The hormone-independent effect of glucose is preserved if the hyperglucagonemia is abolished, but the spontaneous high glucagon level overrules the glucose effect. The results indicate reduced hepatic contribution to the nitrogen-sparing effect of glucose in cirrhotic patients.

Adult↗
PubMed1993

[Nutritional therapy in patients with liver cirrhosis].

Malnutrition is common among patients with cirrhosis of the liver. During the last seven years a total of eight randomized studies concerning the effect of nutritional therapy on the clinical course of these patients have been published. In five of these trials nutritional therapy had an effect on the clinical course (reduced mortality, lessening of ascites and encephalopathy) and in the last three trials only effects on clinical chemistry variables related to liver function could be demonstrated. Overall one-month mortality decreased from 30% in the control groups to 14% in the treated groups, when all the trials were added together (total of 320 patients). Patients with liver cirrhosis have an increased requirement for protein to achieve nitrogen balance. Prescribing diets with restricted protein is no longer warranted in these patients, since protein intolerance is actually uncommon. In patients intolerant of protein, substitution of conventional protein with branched chain amino acids can be effective.

Dietary Proteins↗
PubMed1992

[Effect of 0-(beta-hydroxyethyl)-rutoside (Venoruton) on symptomatic venous insufficiency in the lower limbs].

Forty-three patients recruited from general practice with symptom-producing chronic venous insufficiency in the lower limbs participated in a randomized double-blind clinical trial with Venoruton (300 mg x 3) or a placebo for 28 days. Twenty-eight patients were treated with Venoruton and 19 with a placebo. None of the patients received other forms of treatment for chronic venous insufficiency. No differences were observed between the two groups as regards changes in symptoms (swelling, pain, heaviness, restlessness, itching and cramps) the subjective assessment of the discomfort in the extremities or the circumference of the limbs. Venoruton does not appear to have any effect on chronic venous insufficiency in the lower limbs.

Adult↗
PubMed1992

Effects of an increase in protein intake on hepatic efficacy for urea synthesis in healthy subjects and in patients with cirrhosis.

The efficacy of urea synthesis as measured by functional hepatic nitrogen clearance (i.e., the relation of urea synthesis rate to blood alpha-amino nitrogen concentration) was studied before and after diet protein supplementation in six healthy subjects and five patients with stable cirrhosis (galactose elimination capacity about 60% of control). Daily protein intake was increased for 14 days by a protein-enriched liquid from (mean +/- S.D.) 1.01 +/- 0.32 g/kg body wt. to 1.62 +/- 0.31 g/kg body wt in the control subjects, and from 0.69 +/- 0.21 g/kg body wt. to 1.50 +/- 0.15 g/kg body wt. in the patients with cirrhosis. This increased the hepatic nitrogen clearance from 27 +/- 10 l/h to 39 +/- 15 l/h in the control subjects (p less than 0.05) and from 15 +/- 6 l/h to 21 +/- 7 l/h in the cirrhosis patients (p less than 0.05). There was no effect on the galactose elimination capacity in any group. Compared to the control subjects, the response in hepatic nitrogen clearance relative to the increase in protein intake was reduced by 60% in the patients. Basal glucagon was 75% higher in the patients and increased by 50% during high protein intake (p less than 0.05), but did not parallel the increase in hepatic nitrogen clearance, and it did not change in the control subjects. The study shows that an increase in protein intake selectively increases liver function with regard to disposal of amino nitrogen; the mechanism is qualitatively intact but quantitatively deficient in patients with cirrhosis of the liver, and does not seem to depend on glucagon.

Adult↗