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At least 1,531 records · Page 85Linked to original sources
PubMed1990

[Results of re-thoracotomy for the management of early postoperative complications after bronchoplastic operations].

We reviewed cases of re-thoracotomy performed for early complications after bronchoplastic procedures. One hundred and sixteen bronchoplasties were performed in our department over 20 years. The diseases for which bronchoplasty was undertaken were lung cancer in 102 patients (87.9%), tuberculous stenosis of the bronchus in eight, esophageal cancer in three, and trauma in three. The most frequent postoperative complication was difficulty of expectoration and atelectasis, which generally improved with conservative treatment. Re-thoracotomy was performed for early postoperative intrathoracic complications on 11 patients. The reasons for re-thoracotomy were bronchial anastomotic dehiscence in five cases, obstruction of bronchial anastomosis in two, atelectasis in two, and occlusion of anastomosis of pulmonary arterial angioplasty in two cases. All except two underwent re-thoracotomy within two weeks of the first operations. The operative procedures performed were completion pneumonectomy in six cases, re-bronchoplasty in three, suture of anastomotic dehiscence in two, patch closure of pericardial defect with aspiration of secretions in the atelectatic lobe in one, and partial decortication with suture closure of the alveolar fistula in one. Pedicled omental wrapping was applied to two patients with re-bronchoplasty and one with completion pneumonectomy. Post-operative complications after re-thoracotomy were anastomotic insufficiency in two cases, bronchopleural fistula in two, and pneumonia in one. Two patients underwent a third thoracotomy. There was no anastomotic dehiscence or bronchopleural fistula in the patients with pedicled omental wrapping. One patient died due to bronchopleural fistula within 30 days of re-thoracotomy. Six patients died of recurrence or pneumonia from 39 days to one year after re-thoracotomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchi↗
PubMed1975

Renal tubular acidosis during therapy for diabetic ketoacidosis.

A young woman presented with typical diabetic ketoacidosis. Five hours after insulin had been given hyperchloremic metabolic acidosis developed. This could not be attributed to gastrointestinal loss of bacarbonate, ingestion of HCI or carbonic anhydrase inhibitor, or the administered fluids and electrolytes. The combination of hyperchloremic metabolic acidosis and a urine pH of 5.6 during acidemia prompted specific studies that established the presence of disorders of renal acidification. A transient defect of hydrogen ion secretion in the distal nephron was suggested by the decrease in urine-blood Pco-2 gradient after administration of sodium bicarbonate. Proximal renal tubular acidosis was indicated by the reduced bicarbonate threshold that persisted for approximately 7 weeks.

Acid-Base Equilibrium↗
PubMed1988

"Tolerization" of human T-helper cell clones by chronic exposure to alloantigen: culture conditions dictate autocrine proliferative status but not acquisition of cytotoxic potential and suppressor-induction capacity.

Induction of clonal anergy in T-helper (Th) cells may have a role in regulating immune responses. A model system for studying Th cell tolerization at the clonal level in vitro could be useful for investigating the mechanisms involved. Accordingly, alloreactive helper cells were maintained in culture with interleukin 2 (IL 2) by intermittent stimulation with specific antigen. Regardless of the frequency of antigen stimulation, clones of age less than ca. 35 population doublings (PD) were found to undergo antigen-specific autocrine clonal expansion in the absence of exogenous IL 2. Such young clones (designated as phase I) could therefore not be "tolerized" by frequent exposure to antigen. In contrast, most clones of age greater than ca. 35 PD could be tolerized by frequent exposure to antigen (designated as phase II clones). Their autocrine proliferation was then blocked, although they still recognized antigen specifically as shown by their retained ability to secrete interferon-gamma (IFN-gamma) and granulocyte-macrophage colony stimulating factor (GM-CSF). The mechanism of response failure involved both an inability to upregulate IL 2 receptors in the absence of exogenous IL 2, as well as an inability to secrete IL 2. These defects were not overcome by stimulation with mitogens or calcium ionophore and phorbol esther in place of alloantigen. T-cell receptor, alpha, beta, and gamma-chain gene rearrangements remained identical in phase I and phase II clones. Tolerization of phase II clones could be avoided by increasing the period between antigen exposures. Despite this, whether or not phase II cells were capable of autocrine proliferation, they were found to have acquired the novel function of inducing suppressive activity in fresh lymphocytes. Suppressor-induction was blocked by the broadly reactive MHC class II-specific monoclonal antibody (moAb) TU39, but not by moAb preferentially reacting only with HLA-DR, DQ, or DP. Sequential immunoprecipitation on T-cell clones showed the presence of a putative non-DR, DQ, DP, TU39+ molecule on phase II clones. However, this molecule was also found on phase I clones. The nature of the TU39-blockable suppressor-inducing determinant present on phase II but not on (most) phase I clones thus remains to be clarified. In addition to suppressor-induction activity, phase II clones also acquired lytic potential as measured in a lectin approximation system. Cytotoxic (CTX) potential was also not influenced by the frequency of antigenic stimulation and could be viewed as a constitutive modulation of clonal function.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗
PubMed1988

A Dactylium dendroides morphological mutant defective in D-galactose metabolism.

1. A morphological mutant of the mold Dactylium dendroides was isolated and the phenotype characterized as D-Gal- and L-Ara-. 2. The transport system for D-galactose seemed to be inducible in wild type and mutant and was altered in the mutant. 3. Galactose-1-P-uridylyl transferase activity was absent in the mutant. 4. The levels of intracellular galactose oxidase activity were similar in the wild type and in the mutant, thereby excluding a possible participation of this enzyme in galactose catabolism in the mold. 5. The low level of galactose oxidase activity found in the extracellular medium indicates a defect in galactose oxidase secretion by the mutant.

Arabinose↗
PubMed1981

Lipid and lipoprotein abnormalities in alcoholic liver disease.

Excessive alcohol ingestion results in profound derangements of lipid and lipoprotein metabolism, reflecting the effects of ethanol on peripheral and hepatic lipid metabolism and its toxic effects on hepatic function. The alterations in plasma lipids and lipoproteins are secondary to complex abnormalities of lipoprotein synthesis, secretion and catabolism. The major effects of alcohol include fatty liver secondary to excessive triglyceride synthesis, resulting in an imbalance between synthesis and hepatic secretion; hypertriglyceridemia and hypercholesterolemia; defective plasma cholesterol esterification; and decreased high-density lipoprotein cholesterol. In patients with severe alcoholic hepatitis, the plasma lipoproteins have an abnormal structure and apoprotein composition. Although these changes are usually reversible with abstinence from alcohol (if liver function returns to normal), they indicate serious effects of alcohol on the liver, which may culminate in cirrhosis and hepatic insufficiency. These effects of alcohol on lipids and lipoproteins should be contrasted with the elevation in high-density lipoprotein cholesterol concentration produced by moderate alcohol intake and the possibility that this increase may protect against the development of atherosclerotic disease.

Animals↗
PubMed1993

[Pathophysiologic concepts and protective possibilities in experimental pancreatic lesions].

Experimental pancreatic lesions can be induced by a number of different procedures, e.g. pancreatic hyperstimulation, intraductal application of bile acids, feeding choline deficient diet, obstruction of pancreatic duct, or reducing pancreatic blood flow. The pathogenetic mechanisms leading to pancreatic lesions include basolateral enzyme secretion, acinar cell polarisation defect, intracellular activation of proteases, and the production of free radicals and other active metabolites. The importance of these individual mechanisms in the production and progression of different experimentally-induced pancreatic lesions remains speculative. These pathogenetic concepts have inspired the study of a number of substances likely to protect the pancreas and prevent the pancreatic lesions. This paper gives an overview of the pathogenetic concepts of development of and protection against experimental pancreatic lesions produced in animal models. Special mention has been made of an animal model of pancreatic lesion produced by immunosuppressives.

Animals↗
PubMed1976

Gallstones.

Cholesterol saturation of bile has a primary role in the pathogenesis of gallstone formation. Predisposing factors should be considered. The characteristic features of biliary colic are important to keep in mind, as well as the fact that a history of fatty food intolerance is not of value in the diagnosis of gallstones. The technique of endoscopic retrograde cholangiography is useful for the diagnosis of bile duct stones in jaundiced patients and in patients with a strong clinical history, but in whom findings on oral and intravenous cholangiograms are within normal limits. Improved techniques of operative cholangiography to diminish the incidence of retained gallstones have been developed. Also, choledochoscopy provides a remarkable technique for diagnosis and choledocholithotomy. The dissolution of gallstones with chenodeoxycholic acid is an experimental procedure. This bile acid is thought to act by increasing the chenodeoxycholic acid pool size and decreasing cholesterol synthesis and secretion, thereby reversing the defects responsible for gallstone formation.

Bile Acids and Salts↗
PubMed1996

[Pseudo-idiopathic hypoparathyroidism].

Hypoparathyroidism can exist due to one or more of the following pathogenic mechanisms: 1) Parathyroid Hormone (PTH) deficit, b) biologically inactive PTH, c) PTH antagonists and d) target tissues defects. Biologically inactive PTH secretion, also named pseudo-idiopathic hypoparathyroidism, is an exceptional cause of hypoparathyroidism. We report a case of a patient with this illness. A 71-year-old male with a past history of cataracts since he was 48 was admitted to our hospital. Laboratory data showed a total calcium of 4.82 mg/dl, ionized calcium of 2.72 mg/dl, serum phosphate 5.30 mg/dl, intact PTH 83 pg/ml (N 15-60), osteocalcin 2,4 ng/ml (N 9-30), tubular resorption of phosphate 96% and 1.25 di-hydroxycholecalciferol 7 pg/ml (N 18-78); creatinine and magnesium values were between normal limits. The Ellsworth-Howard test showed a normal response of both urinary c-AMP excretion and phosphaturia to PTH. We review the diagnostic clues of hypoparathyroidism and the value of the Ellsworth-Howard test in order to enable distinction between the several variants of the syndrome.

Aged↗
PubMed1997

Catalytically inactive lecithin: cholesterol acyltransferase (LCAT) caused by a Gly 30 to Ser mutation in a family with LCAT deficiency.

Plasma lecithin:cholesterol acyltransferase (LCAT) plays an important role in early steps of reverse cholesterol transport, i.e., cholesterol efflux from peripheral tissues and cholesterol esterification in HDL. However, structural and functional relationships of LCAT have not been fully elucidated. We described a missense mutation of Gly 30-to-Ser in a patient with classical LCAT deficiency. The proband was homozygous for the mutation and had a very low level of HDL cholesterol (2 mg/dl), with a half of normal LCAT mass (2.75 micrograms/ml), but no detectable or very low LCAT activity in endogenous and exogenous substrate assays. Both his mother and sister were heterozygous for the mutation, and had slightly decreased levels of HDL cholesterol (34 and 36 mg/dl, respectively). Transient expression study using COS cells indicated that mutant cDNA produces similar amounts of media protein as compared to wild type, but no detectable LCAT activity. The missense mutation may result in a near-native conformation without large effects on cellular secretion but a catalytically defective protein. Thus, the N-terminal domain appears crucial for enzymatic activity, in addition to the catalytically active consensus sequence of Gly179 to Gly183 and a putative sterol binding domain of Glu154 to Lys173.

Animals↗
PubMed1997

[Evaluation of 20 years' experience of enuresis in children].

The clinical and urodynamic approach to enuretic children over a period of more than 20 years has allowed the authors to develop a multifactorial pathophysiological concept of this disorder. The main factors involved are psychological, familial, genetic, vesical, due to bladder immaturity, hormonal, due to a defect of nocturnal ADH secretion, hygiene and dietary habits, etc. The sleep factor is predominant in the majority of cases. Although nocturnal enuresis is apparently isolated in many cases, it is often associated with a state of bladder immaturity, sometimes latent during the day, but occurring at night with episodes of detrusor hyperactivity, occurring during various phases of sleep. In practice, the recognition, in children, of these factors, some of which require specific treatments, implies a management combining several of these therapeutic modalities.

Child↗
PubMed1982

Mutations affecting the structure and function of immunoglobulin M.

Using a hybridoma cell line which secretes hapten-specific immunoglobulin M (IgM), we have isolated a variety of mutants which produce abnormal immunoglobulin. Immunoglobulin was tested for the size and composition of the component heavy and light chains and for variable and constant region related functional and serological activities. Some mutants secrete IgM which seems to be defective in hapten binding; others make IgM which appears not to activate complement. Many of the mutants secrete monomeric as opposed to pentameric IgM. In some cases, the defect apparently correlates with structural alterations in the mu heavy chain: partial deletion, polypeptide addition, and abnormal glycosylation have been observed. These mutant cell lines provide a means of identifying the structural basis of IgM function and of studying the biochemistry of IgM synthesis and processing.

Animals↗
PubMed2000

The gonadotropic axis in hyperandrogenic adolescents.

Polycystic ovary syndrome (PCOS) is a common reproductive disorder that is first clinically diagnosable approximately 3 years after menarche. Women with PCOS have exaggerated gonadotropin secretion, with an elevated LH/FSH ratio, as well as an increased frequency and amplitude of LH pulsations. Since the elevated pulse frequency is a marker of unusually rapid hypothalamic GnRH secretion, these results imply a defect at the level of the hypothalamus. Such an abnormality could theoretically be a primary defect that could cause PCOS, and if so, would be expected to be detectable at the onset of puberty. How these abnormalities of hypothalamic and pituitary function relate to other, seemingly disparate, organ defects has not yet been delineated. We studied 99 PCOS patients and 42 normal controls with 8 to 12 hours of q10 min frequent blood sampling. Women with PCOS had significantly elevated mean LH levels, LH pulse amplitude, LH pulse frequency, and LH/FSH ratios compared to normal women. However, these abnormalities were not randomly distributed. All gonadotropin secretion parameters tended to be normal in PCOS patients when measured during the luteal phase or first 7 days after an ovulatory menses. There was a strong inverse relationship of mean LH, LH/FSH ratio, and LH pulse amplitude, but not frequency, with BMI. We hypothesize that this effect of body size occurs at the pituitary level. Several investigators have performed similar investigations in adolescent girls with regular and irregular menstrual cycles. Taken together, this evidence suggests that the gonadotropin defects appear as a very early finding in the development of PCOS, but the presence of abnormalities in both gonadotropin secretion and androgen secretion does not allow one to conclude that the gonadotropin defects are causal. We conclude that gonadotropin defects, particularly excess of serum LH, is a predominant finding in hyperandrogenic women, whether they are young peripubertal adolescents, or older perimenopausal women. Whether there is a primary neuroendocrine abnormality driving excess gonadotropin secretion that causes the hyperandrogenic condition, or whether the excess gonadotropin secretion reflects abnormal feedback of another factor, still remains unknown.

Adolescent↗
PubMed1994

Pathogenesis of glucose intolerance and diabetes mellitus in cirrhosis.

Glucose intolerance and diabetes mellitus are both prevalent in cirrhosis, yet the pathogenesis of impaired glucose metabolism remains unknown. Therefore insulin secretion (hyperglycemic clamp, +125 mg/dl), insulin sensitivity (euglycemic hyperinsulinemic insulin clamp, +10 microU/ml and +50 microU/ml), whole-body glucose oxidation (indirect calorimetry) and glucose turnover ([6,6-2H2]glucose isotope dilution) were evaluated in a homogenous group of cirrhotic patients with glucose intolerance (n = 7) or frank diabetes mellitus (n = 6). The results were compared with those obtained in control subjects (n = 8). In glucose-intolerant patients, whole-body glucose uptake (mainly reflecting glucose utilization by muscle) was significantly impaired in patients during both insulin infusions as a result of decreased stimulation of the two major intracellular pathways of glucose disposal--nonoxidative glucose disposal (i.e., glycogen synthesis) and glucose oxidation. Hepatic glucose production was normal in the basal state and was normally suppressed during stepwise insulin infusion (by 65% and 85%, respectively, p = NS vs. controls). Hyperglycemia-induced increases of plasma C-peptide concentrations were comparable to those in controls (p = NS). In diabetic patients, insulin-mediated glucose uptake was significantly reduced, mainly because of impaired non-oxidative glucose disposal. Glucose oxidation appeared to be reduced, too. Hepatic glucose production was significantly increased in the basal state (3.03 +/- 0.24 vs. 2.34 +/- 0.10 mg/kg min, p < 0.02) and during insulin infusion (+50 microU/ml: 0.67 +/- 0.17 vs. 0.13 +/- 0.08 mg/kg min, p < 0.05) compared with that in controls. Both the first and second phases of beta-cell secretion were significantly reduced in response to steady-state hyperglycemia (both p < 0.01 vs. control values). In conclusion, glucose intolerance in cirrhosis results from two abnormalities that occur simultaneously: (a) insulin resistance of muscle and (b) an inadequate response (even when comparable to that of controls) of the beta-cells to appropriately secrete insulin to overcome the defect in insulin action. Diabetes mellitus in insulin-resistant cirrhotic patients develops as the result of progressive impairment in insulin secretion together with the development of hepatic insulin resistance leading to fasting hyperglycemia and a diabetic glucose tolerance profile.

Adult↗
PubMed1995

Molecular strategies for therapy of cystic fibrosis.

Cystic fibrosis (CF), a lethal disease common to Caucasians, is characterized by a defect in the CF transmembrane conductance regulator and the resulting defective cAMP-regulated Cl- secretion by epithelial cells. Clinical manifestations include both pancreatic and pulmonary insufficiency. Traditional therapeutic modalities address these problems with pancreatic enzyme replacement, vitamins and nutritional supplementation, antibiotics, and respiratory therapy. However, newer therapies directed at the specific underlying defects have emerged. In this review, we discuss agents that increase Cl- secretion via preserved Cl- secretory pathways, such as uridine triphosphate, or that enhance Na+ resorption, such as amiloride, thereby correcting altered airway secretions. We also discuss agents, including deoxyribonuclease (DNase), that directly reduce sputum viscosity. CF is an early target for in vivo gene therapy, since it is a monogenic autosomal recessive disease in which restoration of normal cAMP-regulated Cl- conductance can be achieved by complementation with a normal gene. The early clinical gene therapy therapy work, with gene introduction by both viral and nonviral vectors, is discussed.

Animals↗
PubMed1999

On the pathophysiology of late onset non-insulin dependent diabetes mellitus. Current controversies and new insights.

The development of late onset non-insulin dependent diabetes mellitus (NIDDM) is due to a complicated interplay between genes and environment on one side, and the interaction between metabolic defects in various tissues including the pancreatic beta cell (decreased insulin secretion), skeletal muscle (insulin resistance), liver (increased gluconeogenesis), adipose tissue (increased lipolysis) and possibly gut incretin hormones (defective glucagon like peptide 1 (GLP1) secretion) on the other side. Evidence for a genetic component includes the finding of a variety of metabolic defects in various tissues in non-diabetic subjects with a genetic predisposition to NIDDM, higher concordance rates for abnormal glucose tolerance including NIDDM in monozygotic compared with dizygotic twins, and the more recent demonstration of different NIDDM susceptibility genes at the sites of Insulin Receptor Substrate 1 (IRS1), the beta-3 adrenergic receptor, and the sulfonylurea receptor. However, the latter susceptibility genes only explain a minor proportion of NIDDM in the general population, and the quantitative extent to which genetic versus non-genetic factors contribute to NIDDM is presently unsolved. Environmental components include both an early intrauterine component associated with low birth weight, and later postnatal components including low physical activity, high fat diet, and the subsequent development of obesity and elevated plasma and tissue free fatty acid levels. Our finding of lower birth weights in monozygotic twins compared with their non-diabetic genetically identical co-twins excludes the possibility that the association between NIDDM and low birth weight as demonstrated in several studies may solely be explained by a coincidence between a certain gene causing both a low birth weight and an increased risk of NIDDM. Young first degree relatives of patients with NIDDM are characterized by hyperinsulinaemia and peripheral insulin resistance, which in turn may be explained by a decreased insulin activation of the enzyme glycogen synthase in skeletal muscle. Therefore, a defective skeletal muscle glycogen synthase activation may represent an early phenotypic expression of a genetic defect contributing to an increased risk of later development of NIDDM. However, elderly insulin resistant non-diabetic co-twins (64 years old) of twins with overt NIDDM does not--in contrast to their NIDDM co-twins--have a significantly decreased insulin activation of glycogen synthase in skeletal muscle. This demonstrates that the defective muscle glycogen synthase insulin activation has an apparent non-genetic component, and that this key defect of metabolism can be escaped or postponed even in non-diabetic subjects with a presumably 100% genetic predisposition to NIDDM. The insulin activation of glycogen synthase in skeletal muscle is compensated or apparently normalised in NIDDM patients when studied during their ambient fasting hyperglycaemia and a subsequent isoglycaemic (hyperglycaemic) physiologic insulin infusion. This indicates that the prevailing hyperglycaemia in NIDDM subjects compensates for the defective insulin activation of glycogen synthase present in those subjects when studied during eulycaemia. Our data and those of others also indicates that hyperglycaemia in NIDDM compensates for the defects in insulin secretion, the disproportionately elevated hepatic glucose production, and to some extent for the increased lipid oxidation and the decreased glucose oxidation present in NIDDM patients. Accordingly, NIDDM subjects exhibit all of those defects of metabolism when studied during "experimental decompensation" when the ambient hyperglycaemia is normalized by a prior and later withdrawn intravenous insulin infusion. However, shortly after the withdrawal of the intravenous insulin infusion, the plasma glucose concentration increased spontaneously in the NIDDM patients. (ABSTRACT TRUNCATED)

Age of Onset↗
PubMed1990

[Physiopathology of cystic fibrosis].

Cystic Fibrosis (CF) is the most common lethal genetic autosomic disease in Caucasians. The disease expresses itself in airway and other epithelial cells as a defective chloride ion absorption and secretion. At least, an abnormal cAMP-dependent regulation of an apically located chloride channel has been proposed as the underlying molecular defect. The gene responsible for CF has been identified and predicted to encode a membrane protein termed cystic fibrosis transmembrane conductance regulator (CFTR). The functional role of the predicted protein remains unclear, although strong evidence suggest that it is directly or indirectly involved in regulation of the apical chloride permeability in epithelial cells. This review discusses the fundamental issues currently being investigated in CF.

Bucladesine↗
PubMed1975

Acute-phase insulin secretion and glucose tolerance in young and aged normal men and diabetic patients.

A defect in the early phase of insulin secretion has been proposed as a major determinant of the impaired glucose homeostasis of adult onset diabetes. Since the process of aging is also associated with a deterioration of glucose tolerance, we have measured the acute phase of insulin secretion and glucose disposal rate (KG) after a 20 g glucose pulse in 11 normal, healthy men greater than 65 yr and compared it with the response in 11 nondiabetic men 20-31 yr. The mean fasting plasma sugar levels of the aged subjects (107 mg/dl), tended to be higher than that of the young (94 mg/dl). Comparison of Kg provided clear separation (P less than 0.01) of the old (mean Kg = 0.93) from the young population (mean Kg = 1.95). The acute insulin response to the glucose pulse when expressed either as the area above basal for the 10 min post stimulation or as the mean encremental increase above basal at 3, 4 and 5 min (delta 3-5 IRI) was the same in both timing and magnitude for the old and young subjects. Although our aged subjects had clearly abnormal kg's their acute phase of insulin secretion in response to glucose was normal. Seven noninsulin requiring diabetics with fasting plasma glucose levels greater than 140 mg/dl similarly studied had abnormal kg's (mean = 0.55) but markedly attenuated early release of insulin. Therefore, even though in the diabetics a deficiency of acute phase insulin secretion may have contributed to their impaired kg, in our aged subjects the lack of correlation between kg and a deficiency of acute phase insulin release suggests that factors other than an impairment in the early phase of insulin secretion are responsible for their glucose intolerance or, that there is a dissociation between the biologic and immunologic activity of insulin in these aged subjects.

Adult↗
PubMed1999

[Hepatogenic diabetes: pathophysiology, therapeutic options and prognosis].

About 80% of patients with chronic liver diseases such as cirrhosis are glucose intolerant and some 20-30% eventually develop frank diabetes mellitus. In a given individual it seems impossible to determine whether or not acquired liver diabetes or inherited non-insulin-dependent diabetes mellitus is present. The high prevalence, however, of impaired glucose tolerance and the finding that insulin sensitivity is reduced in nearly all cirrhotic patients before any impairment in glucose tolerance becomes manifest, make it likely that in the majority of patients the hepatic disease is the cause of the development of the hepatogenous diabetes. The insulin resistance resides in muscle and largely results from a defect in glycogen synthesis. Glucose intolerance ensues as a result of two abnormalities that occur simultaneously: insulin resistance of muscle and an inadequate response of the B-cell to appropriately secrete insulin to overcome the defect in insulin action. Diabetes mellitus in insulin-resistant cirrhotic patients develops as a result of a progressive impairment in insulin secretion together with the development of hepatic insulin resistance, leading to fasting hyperglycemia. Until recently, only little was known about the etiology of insulin resistance and impaired insulin secretion. However, most recent studies have shown that prolonged reduction of hyperinsulinemia in cirrhosis normalize insulin-mediated glucose uptake and glycogen synthesis in muscle. These results indicate that chronic hyperinsulinemia causes insulin resistance in cirrhosis and therefore plays a central role in the etiology of the hepatogenous diabetes.

Blood Glucose↗