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Biomedical subjects

John G Kral

Publications and source records attributed to John G Kral.

6 recordsLinked to original sources
PubMed2004

Effects of surgical treatment of the metabolic syndrome on liver fibrosis and cirrhosis.

BACKGROUND: Both weight loss and gastrointestinal surgery for obesity can cause liver disease, making their role in the treatment of obesity-related liver disease controversial. METHODS: Six hundred eighty-nine severely obese women (n=551) and men (n=138), BMI=47+/-9 kg.m(-2) (mean+/-SD), without known liver disease, underwent biliopancreatic diversion (BPD) with liver biopsy. Fourteen patients (2%) had cryptogenic cirrhosis, 11 of whom underwent multiple repeat biopsies. After 38+/-18 kg weight loss, 104 of the 689 patients underwent routine second biopsies during reoperations 41+/-25 months after BPD. All biopsy specimens were graded for steatosis, fibrosis, and inflammation by a blinded hepatopathologist. RESULTS: All 689 patients lost weight accompanied by improvements in the metabolic syndrome. Among the 104 patients who underwent reoperation, severe fibrosis (grade 3-5) decreased in 28 whereas mild fibrosis (grade 1-2) appeared in 42. Increased fibrosis was related to low-normal serum albumin, uncontrolled diarrhea, low intake of alcohol, and menopausal status. Fibrosis and inflammation decreased over time (P<.01). The 11 patients with cirrhosis exhibited decreased fibrosis from a mean grade 5 to grade 3, as well as reduced inflammation, Mallory bodies, and glycogenated nuclei. Seven patients had disappearance and 2 regression of nodules and fibrous bridging. CONCLUSIONS: The metabolic syndrome of obesity is a determinant of liver fibrosis and cirrhosis, treatable by substantial weight loss after malabsorptive surgery.

Adult↗
PubMed2004

Ghrelin: integrative neuroendocrine peptide in health and disease.

OBJECTIVE: Ghrelin is a novel gastric hormone recognized in 1999 as a mediator of growth hormone release. Since growth hormone is anabolic, an important function of ghrelin may be to coordinate energy needs with the growth process. Newly discovered biologic roles of ghrelin imply that it may have other important physiological functions as well. This is a review of recent clinically relevant, yet less well-known, physiologic actions of ghrelin. SUMMARY BACKGROUND DATA: Ghrelin has profound orexigenic, adipogenic, and somatotrophic properties, increasing food intake and body weight. Secreted predominantly from the stomach, ghrelin is the natural ligand for the growth hormone secretagogue receptor in the pituitary gland, thus fulfilling criteria of a brain-gut peptide. The brain-gut axis is the effector of anabolism by regulating growth, feeding, and metabolism via vagal afferents mediating ghrelin signaling. However, the wide tissue distribution of ghrelin suggests that it may have other functions as well. METHODS: Systematic literature review of all PubMed citations between 1999 and August 2003 focusing on clinically relevant biochemical and physiological characteristics of ghrelin. RESULTS: Ghrelin is an important component of an integrated regulatory system of growth and metabolism acting via the vagus nerve, and is implicated in a variety of altered energy states such as obesity, eating disorders, neoplasia, and cachexia. It also enhances immune responses and potentially down-regulates anti-inflammatory molecules. Ghrelin's role as a brain-gut peptide emphasizes the significance of afferent vagal fibers as a major pathway to the brain, serving the purpose of maintaining physiologic homeostasis. CONCLUSIONS: The discovery of ghrelin has increased our understanding of feeding regulation, nutritional homeostasis, and metabolic processes. Further characterization of ghrelin's functions will likely generate new pharmacological approaches to diagnose and treat different disease entities including those related to the over-nutrition of obesity and the catabolic response to surgical trauma.

Brain↗
PubMed2004

Outcome of pregnancies after biliopancreatic diversion.

BACKGROUND: Severe obesity has deleterious effects on fertility and pregnancy outcomes. Although surgery is the best long-term treatment for severe obesity, there is a risk of gestational undernutrition in operated mothers because bariatric surgery reduces nutrient availability. This is a follow-up report of our initial findings regarding pregnancy and neonatal outcomes in biliopancreatic diversion (BPD) patients, with addition of a new cohort of children born to mothers after BPD. METHODS: All women (n = 916) who had successfully undergone BPD in our hospital were mailed a questionnaire containing multiple-choice and essay questions concerning gynecologic and obstetric history, and pregnancy and neonatal outcomes in both preoperative and postoperative pregnancies. Patients operated between 1984 and 1995 (n = 568) were mailed an additional questionnaire regarding children's weight and height progress, and school performance. Perinatal records from our patients' obstetric clinics were also reviewed. RESULTS: The questionnaire was completed by 783 women (85.5%). 251 postoperative pregnancies in 132 women resulted in 166 infants by 109 mothers. 47.0% of patients who were unable to become pregnant preoperatively were successful postoperatively. 90 out of 109 women (82.6%) reported an appropriate weight gain (9.1 +/- 5.9 kg) during postoperative pregnancies. The incidence of fetal macrosomia decreased from 34.8 to 7.7%, with a concomitant increase in normal-weight babies from 62.1 to 82.7%. The elevated miscarriage rate (26.0%) in these obese women persisted after surgery. CONCLUSION: Major weight loss following BPD improves the reproductive function of severely obese women. BPD provides major beneficial effects for both mother and child, including normalization of gestational weight changes, reduction of fetal macrosomia, and normalization of the infant's birth-weight. Our results speak in favor of delaying pregnancy in obese women until after the substantial surgical weight loss has occurred.

Adolescent↗
PubMed2003

Binge eating as a major phenotype of melanocortin 4 receptor gene mutations.

BACKGROUND: Obesity, a multifactorial disease caused by the interaction of genetic factors with the environment, is largely polygenic. A few mutations in these genes, such as in the leptin receptor (LEPR) gene and melanocortin 4 receptor (MC4R) gene, have been identified as causes of monogenic obesity. METHODS: We sequenced the complete MC4R coding region, the region of the proopiomelanocortin gene (POMC) encoding the alpha melanocyte-stimulating hormone, and the leptin-binding domain of LEPR in 469 severely obese white subjects (370 women and 99 men; mean [+/-SE] age, 41.0+/-0.5 years; body-mass index [the weight in kilograms divided by the square of the height in meters], 44.1+/-2.0). Fifteen women and 10 men without a history of dieting or a family history of obesity served as normal-weight controls (age, 47.7+/-2.0 years; body-mass index, 21.6+/-0.4). Detailed phenotypic data, including information on body fat, resting energy expenditure, diet-induced thermogenesis, serum concentrations of leptin, and eating behavior, were collected. RESULTS: Twenty-four obese subjects (5.1 percent) and one control subject (4 percent) had MC4R mutations, including five novel variants. Twenty of the 24 obese subjects with an MC4R mutation were matched for age, sex, and body-mass index with 120 of the 445 obese subjects without an MC4R mutation. All mutation carriers reported binge eating, as compared with 14.2 percent of obese subjects without mutations (P<0.001) and 0 percent of the normal-weight subjects without mutations. The prevalence of binge eating was similar among carriers of mutations in the leptin-binding domain of LEPR and noncarriers. No mutations were found in the region of POMC encoding alpha melanocyte-stimulating hormone. CONCLUSIONS: Binge eating is a major phenotypic characteristic of subjects with a mutation in MC4R, a candidate gene for the control of eating behavior.

Adolescent↗
PubMed2003

Adipose tissue quantification by imaging methods: a proposed classification.

Recent advances in imaging techniques and understanding of differences in the molecular biology of adipose tissue has rendered classical anatomy obsolete, requiring a new classification of the topography of adipose tissue. Adipose tissue is one of the largest body compartments, yet a classification that defines specific adipose tissue depots based on their anatomic location and related functions is lacking. The absence of an accepted taxonomy poses problems for investigators studying adipose tissue topography and its functional correlates. The aim of this review was to critically examine the literature on imaging of whole body and regional adipose tissue and to create the first systematic classification of adipose tissue topography. Adipose tissue terminology was examined in over 100 original publications. Our analysis revealed inconsistencies in the use of specific definitions, especially for the compartment termed "visceral" adipose tissue. This analysis leads us to propose an updated classification of total body and regional adipose tissue, providing a well-defined basis for correlating imaging studies of specific adipose tissue depots with molecular processes.

Adipose Tissue↗