glycogen and Diarrhea

Giardia intestinalis is the causative agent of human giardiasis, a common diarrheal illness worldwide. Despite its global distribution and prevalence, many questions regarding its basic biology and metabolism remain unanswered. In this study, we examine the accumulation and degradation of glycogen, an important source of stored carbon and energy, during the in vitro growth and differentiation of G. intestinalis . We report that, as G. intestinalis progresses through its growth cycle, cultures of trophozoites accumulate glycogen during the lag and early logarithmic phases of growth and then utilize this compound during their remaining logarithmic growth. As cultures enter the stationary phase of growth, they re-accumulate glycogen stores. The activity of glycogen phosphorylase, an enzyme involved in glycogen metabolism, also varied throughout in vitro trophozoite growth. During the in vitro induction of trophozoite differentiation into water-resistant cyst forms, the cultures initially accumulated stores of glycogen which diminished throughout transition to the cyst form. This observation is suggestive of a role for glycogen in the differentiation process. These studies represent the first thorough analysis of changes in glycogen content and glycogen phosphorylase activity during G. intestinalis growth and differentiation.

Topics: Culture Media; Diarrhea; Giardia lamblia; Giardiasis; Glycogen; Glycogen Phosphorylase; Humans

In the present work, the authors' previous studies of a "distant action", exerted by an intestinal pathogen (Cryptosporidium parvum) on the liver of experimentally infected baby rats, were extended to include shifts in the quantity of glycogen, protein and nuclear DNA in the host liver at different degrees of infection. One of the outcomes of this work is the discovery of a very quick response of hepatocytes and a high sensitivity of rat liver to parasitic invasion even at a weak intensity of infection. 85-90 h after oocyst feeding to rats, glycogen quantity in their livers was 2.5 times lower that in the control. This suggests that the infected host liver worked under energetic starvation conditions. The proposed coefficients of general infection (I) and infection with intracellular stages (F) made it possible to distinguish between the total abundance of parasites in the host intestine during the whole period of infection, and the number of feeding intracellular stages available by the moment of autopsy. The glycogen amount in rat hepatocytes does not depend on I, and negatively correlates with F. Unlike, the protein content in hepatocytes positively correlates with I, being independent of F. Despite the obvious deficiency of amino acids in the infected rats, as a consequence of cryptosporidiosis-induced malabsorption, the protein synthesis in their hepatocytes was not at all inhibited but, on the contrary, much activated. This is a most characteristic feature of the distant action of C. parvum on the liver of parasitized host. With C. parvum infection, the share of polyploid hepatocytes does not correlate with either I, or F. However, compared to the control, the mean values of relative numbers of polyploid cells in weakly, moderately, and heavily infected animals (according to I values) were higher by 20, 100 and 100%, respectively. In hepatocyte nuclei of C. parvum infected rats, the total area of nucleoli increases almost by 30%. The above changes are discussed in terms of both the liver compensatory response to the existing pathology (diarrhea), and the host-parasite relationships. Studies into the distant action of an intestinal pathogen (C. parvum) on non-intestinal organs (liver) of the infected host may be qualified as a new and original approach to pathogenesis of protozoan infections (coccidioses sensu lato), to which young host specimens are known to be most susceptible.

Topics: Animals; Animals, Suckling; Cell Nucleolus; Cell Nucleus; Cryptosporidiosis; Cryptosporidium parvum; Diarrhea; Disease Models, Animal; Glycogen; Hepatocytes; Intestine, Small; Polyploidy; Proteins; Rats; Rats, Wistar

To develop and evaluate the efficacy of diabetes-targeted cell therapies in humans, a reliable model in larger animals is highly desirable. This article reports the surgical technique of total pancreatectomy in pigs and the biochemical analysis of the characteristics of totally pancreatectomized pigs.. Surgical total pancreatectomy was conducted in 23 pigs. Blood glucose, insulin, biochemistries, activity index, and intravenous glucose tolerance test (IVGTT) were examined to assess the pathophysiological profiles of diabetic pigs.. A total of 14 pigs successfully underwent total pancreatectomy without requiring biliary reconstruction and were analyzed in the present study. Activity index was decreased from day 5 on and the mean survival of totally pancreatectomized pigs was 7.6 +/- 2.7 days. No endogenous insulin secretion was confirmed in these pigs. Pigs which received total pancreatectomy demonstrated significantly higher levels of ketone bodies. IVGTT performed within 4 days after total pancreatectomy showed a spontaneous decrease in blood glucose levels despite an absence of endogenous insulin secretion. IVGTT on day 5 or later showed continued hyperglycemia in pigs with total pancreatectomy. Histological examination showed atrophy of hepatocytes and decreased glycogen storage in the liver and decreased mucus production of the small intestine.. This article describes a porcine model of diabetes created by total pancreatectomy and it analyzes the pathophysiological profiles in the animals. The present study has suggested that IVGTT on day 5 or later after total pancreatectomy is a reliable method to evaluate the efficacy of cell therapies.

Topics: Alanine Transaminase; Animals; Area Under Curve; Aspartate Aminotransferases; Atrophy; Blood Glucose; Blood Urea Nitrogen; Body Weight; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Diarrhea; Disease Models, Animal; Glucose Tolerance Test; Glycogen; Hepatocytes; Intestinal Mucosa; Ketone Bodies; L-Lactate Dehydrogenase; Liver; Pancreatectomy; Potassium; Swine