glycogen and Malaria

Fasting is an important risk factor for hypoglycemia in children with malaria or pneumonia. Young children are more at risk because of impaired endogenous glucose production presumably due to smaller liver glycogen stores. The aim of this study was to measure the effect of a bolus of glucagon on glucose kinetics, as an indicator of glycogen content, in fasted children with malaria and pneumonia.. After a 16-h controlled fast, plasma glucose concentration and endogenous glucose production were measured using [6,6-2H2]glucose in six children with severe malaria and 12 children with severe pneumonia who were 1-5 years of age before and after a bolus glucagon.. Basal glucose concentration and endogenous glucose production were higher in children with malaria, p=0.034 and p=0.010, respectively. After glucagon, the increase in the plasma glucose concentration was higher in children with malaria (52±26% vs. 31±23%, p=0.029). Also, the increase in glucose production was higher in children with malaria (106±42% vs. 70±52%, p=0.023). There were no differences in the fasting duration or duration of illness.. This is the first study to show infectious disease-related differences in the adaptation of glucose metabolism to fasting in young children. It was found that basal glucose concentration and endogenous glucose production were higher in children with malaria. The increase in plasma glucose concentration and endogenous glucose production in response to glucagon was higher in children with malaria, indicating smaller glycogen stores in children with pneumonia.

Topics: Adaptation, Physiological; Blood Glucose; Child, Preschool; Fasting; Female; Gastrointestinal Agents; Glucagon; Glycogen; Humans; Hypoglycemia; Infant; Insulin; Liver; Malaria; Male; Models, Biological; Pilot Projects; Pneumonia; Risk Factors; Suriname

One-hundred-and-sixty-eight male Sprague-Dawley rats (weight range 90-150 g) were randomly divided into four separate experimental groups: Control (. Results showed that Tz mono-infection and Tz + Pb co-infection did not have blood glucose lowering effect in the host as expected. This points to other possible mechanisms through which tissue-dwelling parasites up-regulate the glucose store without decreasing the blood glucose concentration as exhibited by the absence of hypoglycaemia in Tz + Pb co-infection group. Hypoinsulinemia and an increase in liver glycogen content was observed in Tz mono-infection and Tz + Pb co-infection groups of which the triggering mechanism remains unclear.. To get more insights into how glucose, insulin and glycogen profiles are affected during plasmodium-helminths co-infections, further studies are recommended where other tissue-dwelling helminths such as

Topics: Animals; Blood Glucose; Coinfection; Glucose; Glycogen; Humans; Insulin; Insulin, Regular, Human; Lead; Malaria; Male; Plasmodium berghei; Rats; Rats, Sprague-Dawley; Trichinella

Malaria reduces host fitness and survival by pathogen-mediated damage and inflammation. Disease tolerance mechanisms counter these negative effects without decreasing pathogen load. Here, we demonstrate that in four different mouse models of malaria, adrenal hormones confer disease tolerance and protect against early death, independently of parasitemia. Surprisingly, adrenalectomy differentially affects malaria-induced inflammation by increasing circulating cytokines and inflammation in the brain but not in the liver or lung. Furthermore, without affecting the transcription of hepatic gluconeogenic enzymes, adrenalectomy causes exhaustion of hepatic glycogen and insulin-independent lethal hypoglycemia upon infection. This hypoglycemia is not prevented by glucose administration or TNF-α neutralization. In contrast, treatment with a synthetic glucocorticoid (dexamethasone) prevents the hypoglycemia, lowers cerebral cytokine expression and increases survival rates. Overall, we conclude that in malaria, adrenal hormones do not protect against lung and liver inflammation. Instead, they prevent excessive systemic and brain inflammation and severe hypoglycemia, thereby contributing to tolerance.

Topics: Adrenal Glands; Adrenalectomy; Animals; Blood Glucose; Brain; Corticosterone; Cytokines; Dexamethasone; Disease Models, Animal; Epinephrine; Glucocorticoids; Glycogen; Hormones; Hydrocortisone; Hypoglycemia; Inflammation; Liver; Lung; Malaria; Mice; Mineralocorticoids; Norepinephrine; Plasmodium berghei; Plasmodium chabaudi; Survival Rate

The present study investigated the effects of transdermally delivered oleanolic acid (OA) monotherapy and in combination with chloroquine (CHQ) on malaria parasites and glucose homeostasis of P. berghei-infected male Sprague-Dawley rats. Oral glucose test (OGT) responses to OA-pectin patch and CHQ-OA combination matrix patch were monitored in non-infected and infected rats. To evaluate the short-term effects of treatment, percentage parasitaemia, blood glucose, glycogen and plasma insulin were monitored in separate groups of animals treated with either OA-patch monotherapy or CHQ-OA combination pectin patch over a 21-days period. Animals treated with drug-free pectin and CHQ acted as untreated and treated positive controls, respectively. Infected control rats exhibited significantly increased parasitaemia which was accompanied by hypoglycaemia. Both OA monotherapy and CHQ-OA combination therapy reduced and cleared the malaria parasites within a period of 4 and 3 days, respectively. Compared to respective controls groups, OGT responses of animals treated with OA monotherapy or CHQ-OA combination therapy exhibited lower blood glucose levels at all time points. A once-off transdermal application of OA-patch or CHQ-OA combination patch significantly improved blood glucose concentrations inducing any changes in insulin concentration. Transdermal OA used as a monotherapy or in combination with CHQ is able to clear and reduce the malaria parasites within a shorter period of time without eliciting any adverse effects on glucose homeostasis of P. berghei-infected rats.

Topics: Administration, Cutaneous; Animals; Antimalarials; Blood Glucose; Chloroquine; Drug Therapy, Combination; Glycogen; Homeostasis; Insulin; Malaria; Male; Oleanolic Acid; Parasitemia; Plant Extracts; Plasmodium berghei; Rats; Rats, Sprague-Dawley; Syzygium

Topics: Animals; Brain; Disease Models, Animal; Glycogen; Haplorhini; Histocytochemistry; Kidney; Lipids; Liver; Malaria; Monkey Diseases; Organ Size; Plasmodium falciparum; Spleen; Staining and Labeling

Topics: Animals; Blood Glucose; Glycogen; Glycogenolysis; Liver; Liver Glycogen; Malaria; Mice; Plasmodium berghei

Topics: Animals; Blood Glucose; Glycogen; Humans; Macaca mulatta; Malaria; Plasmodium knowlesi

Topics: Animals; Cortisone; Glycogen; Glycogenolysis; Liver; Malaria; Plasmodium berghei; Prednisolone; Prednisone; Rats

Topics: Animals; Carbohydrate Metabolism; Glycogen; Liver; Malaria; Plasmodium berghei; Rats

Topics: Animals; Glycogen; Malaria; Plasmodium berghei; Rats