Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To aid understanding of markers of disease and predictors of outcome in alcohol-exposed systems, we undertook a literature survey of more than 700 articles to view the morphological characteristics and the clinical and experimental epidemiology of the Mallory body. Mallory bodies are filaments of intermediate diameter that contain intermediate filament components (e.g., cytokeratins) observable by conventional light microscopy or immunohistochemical methods, identical in structure regardless of initiating factors or putative pathogenesis. Although three morphological types can be identified under electron microscopy (with fibrillar structure parallel, random or absent), they remain stereotypical manifestations of hepatocyte injury. A summary of the conditions associated with Mallory bodies in the literature and their validity and potential etiological relationships is presented and discussed, including estimates on the combined light microscopic and immunohistochemical prevalences and kinetics. Emphasis is placed on proper confounder control (in particular, alcohol history), which is highly essential but often inadequate. These conditions include (mean prevalence of Mallory bodies in parentheses): Indian childhood cirrhosis (73%), alcoholic hepatitis (65%), alcoholic cirrhosis (51%), Wilson's disease (25%), primary biliary cirrhosis (24%), nonalcoholic cirrhosis (24%), hepatocellular carcinoma (23%), morbid obesity (8%) and intestinal bypass surgery (6%). Studies in alcoholic hepatitis strongly suggest a hit-and-run effect of alcohol, whereas other chronic liver diseases show evidence of gradual increase in prevalence of Mallory bodies with severity of hepatic pathology. Mallory bodies in cirrhosis do not imply alcoholic pathogenesis. Obesity, however, is associated with alcoholism and diabetes, and Mallory bodies are only present in diabetic patients if alcoholism or obesity complicates the condition. In addition, case studies on diseases in which Mallory bodies have been identified, along with pharmacological side effects and experimental induction of Mallory bodies by various antimitotic and oncogenic chemicals, are presented. Mallory bodies occur only sporadically in abetalipoproteinemia, von Gierke's disease and focal nodular hyperplasia and during hepatitis due to calcium antagonists or perhexiline maleate. Other conditions and clinical drug side effects are still putative. Finally, a variety of experimental drugs have been developed that cause Mallory body formation, but markedly different cell dynamics and metabolic pathways may raise questions about the relevance of such animal models for human Mallory body formation. In conclusion, the Mallory body is indicative but not pathognomonic of alcohol involvement. A discussion on theories of development and pathological significance transcending the clinical frameworks will be presented in a future paper.
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PMID:The Mallory body: morphological, clinical and experimental studies (Part 1 of a literature survey). 792 9

The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
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PMID:Positional cloning of the mouse obese gene and its human homologue. 798 30

Nowadays, incisional hernias are still one of the more common complications of abdominal surgical procedures. A population, at high risk of developing an incisional hernia, has been chosen for this study, namely patients suffering from morbid obesity. The aim of the study was to compare prospectively the incidence of incisional hernias in 2 groups of patients operated upon for morbid obesity (Vertical Silicone Ring Gastroplasty) with or without intraperitoneal polyglactin mesh. Patients were randomly assigned in the 2 groups. For this preliminary study, 112 patients operated upon before 01/04/1992 were selected; the mean follow-up period was 28.3 months (S.D.:5.7); 81 patients have been reviewed personally, 31 interviewed by phone call or mail. The 2 groups of patients were not significantly different as regarding age, sex, weight, body mass index, diabetes and wound infection. Sixteen incisional hernias were observed in the group with mesh and 17 in the group without mesh. According to these preliminary results, there is no argument for recommending the use of the polyglactin mesh in the prevention of postoperative incisional hernias, in obese patients.
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PMID:Use of an absorbable polyglactin mesh for the prevention of incisional hernias. 857 17

Impaired glucose tolerance and overt diabetes are more frequent in presence than in absence of obesity. In obese subjects, glucose tolerance can be maintained within the normal range by compensating for insulin resistance by peripheral hyperinsulinism, the latter resulting from both increased insulin secretion and reduced insulin clearance. Impaired glucose tolerance is observed when insulin resistance is associated to impaired first-phase insulin response, which results in a significant increase in plasma glucose levels and a late insulin hyperresponsiveness. Both hyperinsulinaemia and hyperglycaemia are then able to overcome peripheral insulin resistance and impaired glucose disposal. When a more marked defect in insulin secretion is present, hyperglycaemia progresses, probably due to an additional participation of impaired suppression of hepatic glucose output. Overt diabetes then occurs with persistent post-absorptive hyperglycaemia. All these abnormalities can be reversed after a marked weight loss and recovery of ideal body weight, arguing for acquired rather than inherited metabolic defects in presence of morbid obesity. If a sufficient weight reduction can not be obtained, pharmacological approaches may be considered to improve insulin resistance of obese subjects, especially those with impaired glucose tolerance or overt diabetes.
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PMID:Glucose metabolism in obese subjects: lessons from OGTT, IVGTT and clamp studies. 858 Oct 72

The mouse obese (ob) gene product (leptin), expressed specifically in adipose cells, regulates energy balance in mice. Both mouse diabetes (db) and rat fatty (fa) gene products are thought to play major roles in leptin signaling pathways in the hypothalamic area. Mutations of these genes in murines result in marked obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. Reported herein are the cloning and sequencing of one of spliced variant forms of rat leptin receptor (OB-R) cDNA with a short intracellular domain. In the Zucker (fa/fa) rat, no changes in either the gene structure or the expression levels were observed. However phenotype-linked nucleotide alteration exists in the cDNA from Zucker (fa/fa) rat, which results in an amino acid substitution.
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PMID:Phenotype-linked amino acid alteration in leptin receptor cDNA from Zucker fatty (fa/fa) rat. 863 68

A total of 325 patients, aged 80 to 92 (mean 82), underwent cardiac operations with cardiopulmonary bypass over a 4-year period (1991-1995). Hypothermia (22 degrees C) and hyperkalemic cardioplegia were used in each. Coronary bypass procedures only (Group I) were performed in 255 patients with 22 early deaths (8.6%), and the average number of grafts was 3.7 per patient. Single or double valve replacement, with coronary bypass (Group II) was performed in 46 patients, with six early deaths (13%). Single or double valve replacement, without coronary bypass (Group III) was performed in 24 patients, with two early deaths (8.3%). Total hospital mortality was 30 deaths in 325 patients (9.2%). Fifty-six procedures (22%) from Group I and four (9%) from Group II were performed as emergencies, and all operations in Group III were elective. Seventy-two patients (27%) from Group I, 18 patients (39%) from Group II, and nine patients (37%) from Group III had major complications including renal failure, cerebrovascular accident, myocardial infarction, postoperative hemorrhage, sepsis, and ventilatory dependency. Mean hospital stay was 10.5 days for Group I, 13.3 days for Group II, and 15.2 days for Group III, with an overall mean of 13 days (range, 6-52) days. Higher mortality was related to a cardiac index <1.8, cardiogenic shock, emergency operation, creatinine >2.0, and morbid obesity. Mean left ventricular ejection fractions were 0.51 for Group I, 0.45 for Group II, and 0.49 for Group III. Preoperative risk factors associated with a higher mortality included hypertension, smoking, diabetes, and pulmonary hypertension. Two hundred seventy-two of the 299 operative survivors were followed for a mean of 18 (range, 3-52) months. The actuarial survival of octogenarians is 92 per cent, 80 per cent, and 65 per cent at 1, 3, and 5 years, respectively, and of the patients surviving operation it was 85 per cent, 70 per cent, and 55 per cent at 1, 3, and 5 years, respectively. At postoperative follow up, 80 per cent of the survivors reported an active functional status, and there was a low incidence of cardiac-related deaths.
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PMID:Coronary artery bypass and valve replacement in octogenarians. 889 18

Morbid obesity is related to a severe decrease in life expectancy. No medical or dietary treatment offers an alternative to control hypertension, apnea syndrome, orthopedic diseases, ..., caused by overweight. With respect to a serious preoperative evaluation and a severe selection (psychologic, dietetic, ...) Silastic Ring Vertical Gastroplasty is considered in our experience (more than 300 cases) and in the literature as the gold standard for surgical treatment of obesity. The long term follow-up (24-66 months) of 100 consecutive operated patients shows a positive response on hypertension (96%), apnea syndrome (92%), diabetes (85%), gastroesophageal reflux (76%), orthopedic diseases (74%) and cardiorespiratory insufficiency (74%). Considering our experience in the medical and surgical management of patients operated in our department or referred from other centers for complications after different procedures, we actually propose SRVG as the treatment of choice for morbid obesity.
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PMID:[The treatment of morbid obesity with gastroplasty]. 892 52

Obesity is a common component of non-insulin-dependent diabetes mellitus (NIDDM) and plays an important role in the development of insulin resistance and hyperinsulinemia. Prader-Willi syndrome (PWS) has been associated with morbid obesity and an increased propensity for early development of NIDDM. It has been assumed that the etiology for this increased rate of NIDDM is related to the morbid obesity and concomitant insulin resistance, but this remains controversial. To shed light on the glucoregulatory mechanisms in PWS, we studied both pediatric and adult PWS patients with normoglycemia. The objectives of our study were (1) to examine glucose, insulin, and C-peptide responses to oral (OGTT) and intravenous (IVGTT) glucose tolerance tests; (2) to characterize acute first- and second-phase insulin secretion during an IVGTT; (3) to assess hepatic insulin extraction (HIE) and insulin clearance (IC) in PWS subjects; and (4) to determine whether beta-cell function in PWS is age-dependent. These results in PWS were compared with values obtained in age-, sex-, and body mass index (BMI)-matched non-PWS obese controls. Three groups were studied. Group I consisted of nine PWS subjects under the age of 13 years and 22 age-, sex-, weight-, and puberty stage-matched obese subjects who underwent OGTT. Group II consisted of 14 adult PWS subjects and 10 age-, weight-, and BMI-matched obese adults who underwent OGTT. Group III consisted of nine adult PWS subjects and eight age-, sex-, and weight-matched obese adults who underwent frequently sampled IVGTT (FSIVGTT). During the OGTT in the pediatric group, fasting (86 +/- 3 v 89 +/- 2 mg/dL), peak (144 +/- 11 v 147 +/- 4 mg/dL), and total area under the curve (AUC) (6,984 +/- 1,320 v 6,963 +/- 615 mg/dL x min) glucose levels were not significantly different in PWS versus obese children, respectively. In contrast, fasting (20 +/- 6 v 37 +/- 4 microU/mL), peak (114 +/- 24 v 214 +/- 23 microU [correction of mU]/mL), and total AUC (12,673 +/- 2,176 v 26,734 +/- 2,608 microU/mL microU/mL min) insulin levels were significantly lower in pediatric PWS. During the OGTT in the adult groups, neither fasting insulin (16.7 +/- 2.8 v 13.5 +/- 2.5 microU/mL) nor total AUC for insulin (10,664 +/- 1,955 v 11,623 +/- 1,584 microU/mL x min) were significantly different in adult PWS and obese groups. During the IVGTT in adults, both first-phase (138 +/- 42 v 454 +/- 102 microU/mL x min) and second-phase (295 +/- 66 v 1,015 +/- 231 microU/mL x min) insulin release were significantly reduced in PWS subjects despite similar glucose levels. Similarly, first-phase (8.6 +/- 2.3 v 21 +/- 4.6 ng/dL x min) and second-phase (47 +/- 4.6 v 75 +/- 14 ng/dL x min) C-peptide responses were also significantly reduced in PWS subjects. In contrast, mean HIE and IC was 33% higher in PWS subjects versus obese controls (15.4 +/- 1.5 v 10.3 +/- 1.6). Similarly, poststimulation HIE and IC was significantly greater (5.2 +/- 0.8 v 2.4 +/- 0.4) in the PWS group compared with the obese group (P < .01). In summary, this study demonstrates that nondiabetic PWS subjects manifest (1) a reduced beta-cell response to glucose stimulation, (2) a significantly increased HIE compared with obese controls, and (3) a dissociation of obesity and insulin resistance, in contrast to normal obese subjects. We conclude that glucoregulatory mechanisms are different in obese PWS versus non-PWS subjects.
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PMID:Characterization of alterations in glucose and insulin metabolism in Prader-Willi subjects. 896 85

A patient with morbid obesity and insulin-dependent diabetes was admitted to the surgical intensive care unit, four days status postsurgical repair of an umbilical hernia. A pulmonary embolus (PE) was diagnosed by ventilation/perfusion scan and confirmed by transthoracic echocardiogram. A right ventricular ejection fraction/volumetric/oximetry pulmonary artery catheter revealed a very low ejection fraction and cardiac index. Systemic urokinase therapy was initiated and the patient improved considerably over the ensuing 12 hours. Anesthesiologists must be able to diagnose the signs and symptoms of PE and should be familiar with treatment modalities to reverse right ventricular dysfunction. Review of the literature regarding thrombolytic therapy in the perioperative period indicates potential benefit in select patients.
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PMID:Thrombolytic therapy for treatment of pulmonary embolism in the postoperative period: case report and review of the literature. 898 98

The sulfonylurea receptor (SUR) is a key component in glucose-stimulated insulin secretion. Obesity and NIDDM are frequently associated and share some metabolic abnormalities, suggesting that they might also share some susceptibility genes. Thus, the SUR encoding gene is a plausible candidate for a primary pancreatic beta-cell defect and thus for hyperglycemia and weight gain. Through association and linkage studies, we have investigated the potential role of the SUR gene in families with NIDDM and in two independent sets of morbidly obese families. The exon 22 T-allele at codon 761 was more common in patients with NIDDM (7.7%) and morbid obesity (7.8%) than in control subjects (1.8%, P = 0.030 and P = 0.023, respectively). This variant was associated with morbid obesity (odds ratio 3.71, P = 0.017) and NIDDM (odds ratio 2.20, P = 0.04; association dependent on BMI). Although the frequencies for intron 24 variant were similar in all groups, morbidly obese patients homozygous for the c-allele had a more deleterious form of obesity. Sib-pair linkage studies with NIDDM in French Caucasian families gave no evidence for linkage to the SUR locus. However, in one set of the obese families, we found an indication for linkage with a SUR-linked microsatellite marker (D11S419, P = 0.0032). We conclude that in Caucasians, the SUR locus may contribute to the genetic susceptibility to NIDDM and obesity.
Diabetes 1997 Apr
PMID:Genetic studies of the sulfonylurea receptor gene locus in NIDDM and in morbid obesity among French Caucasians. 907 12


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