glycogen and Malnutrition

Homeostasis of nutrient metabolism is critical for maintenance of the normal physiologic status of the cell and the integral health of humans and mammals. In vivo, there is a highly efficient and precise process involved in nutrient recycling and organelle cleaning. This process is named autophagy, and it can be induced in response to the dynamic change of nutrients. When cells face nutritional stress, such as stress caused by nutrient deficiency or nutrient excess, the autophagy pathway will be activated. Generally, when nutrients are withdrawn, cells will sense the signs of starvation and respond. AMP-activated protein kinase and the mammalian target of rapamycin, two of the major metabolic kinases, are responsible for monitoring cellular energy and the concentration of amino acids, respectively. Nutrient excess also induces autophagy, mainly via the reactive oxygen species and endoplasmic reticulum stress pathway. When nutritional stress activates the autophagy pathway, the nutrients or damaged organelles will be recycled for cell survival. However, if autophagy is overwhelmingly induced, autophagic cell death will possibly occur. The balance of the autophagy induction is the crucial factor for cell survival or death. Herein, we summarize the current knowledge on the induction of autophagy, the autophagy response under nutritional stresses, and autophagic cell death and related diseases, which will highlight the process of nutritional stress-induced autophagy and its important physiologic and/or pathologic roles in cell metabolism and diseases, and shed light on the research into the mechanism and clinical applications of autophagy induced by nutritional stresses.

Topics: Amino Acids; AMP-Activated Protein Kinases; Autophagy; Carbohydrate Metabolism; Endoplasmic Reticulum Stress; Energy Metabolism; Glycogen; Humans; Lipid Metabolism; Malnutrition; Mechanistic Target of Rapamycin Complex 1; Reactive Oxygen Species; Signal Transduction; Stress, Physiological

Insulin resistance and obesity are components of the metabolic syndrome that includes development of cardiovascular disease and diabetes with advancing age. The thrifty phenotype hypothesis suggests that offspring of poorly nourished mothers are predisposed to the various components of the metabolic syndrome due to adaptations made during fetal development. We assessed the effects of maternal nutrient restriction in early gestation on feeding behavior, insulin and glucose dynamics, body composition, and liver function in aged female offspring of ewes fed either a nutrient-restricted [NR 50% National Research Council (NRC) recommendations] or control (C: 100% NRC) diet from 28 to 78 days of gestation, after which both groups were fed at 100% of NRC from day 79 to lambing and through lactation. Female lambs born to NR and C dams were reared as a single group from weaning, and thereafter, they were fed 100% NRC recommendations until assigned to this study at 6 yr of age. These female offspring were evaluated by a frequently sampled intravenous glucose tolerance test, followed by dual-energy X-ray absorptiometry for body composition analysis prior to and after ad libitum feeding of a highly palatable pelleted diet for 11 wk with automated monitoring of feed intake (GrowSafe Systems). Aged female offspring born to NR ewes demonstrated greater and more rapid feed intake, greater body weight gain, and efficiency of gain, lower insulin sensitivity, higher insulin secretion, and greater hepatic lipid and glycogen content than offspring from C ewes. These data confirm an increased metabolic "thriftiness" of offspring born to NR mothers, which continues into advanced age, possibly predisposing these offspring to metabolic disease.

Topics: Aging; Animals; Body Composition; Eating; Female; Glucose; Glucose Tolerance Test; Glycogen; Insulin; Insulin Resistance; Insulin Secretion; Lipids; Liver; Malnutrition; Maternal Nutritional Physiological Phenomena; Obesity; Sheep

Exposure to maternal undernutrition during development increases the risk for neurological and cognitive defects. However, little is known about the underlying mechanisms involved. Peripheral responses to insulin are increased following food-restriction, thus the possibility arises that brain insulin actions are affected by undernutrition, causing damages to the higher cerebral functions. In this study, we examined the effects of early undernutriton on molecular targets of insulin actions such as glucose transporters, glycogen, glycogen synthase kinase-3 (GSK3) and mitogen-activated protein kinases, as well as proteins involved in apoptosis in the cortex from 10-day-old rats. We show that undernutrition results in an enhanced glycogen content which is confined to astrocytes, according to our histochemical approaches. Cortical phospho-GSK3 is also increased. In addition to glycogen synthesis, GSK3 regulates crucial cellular processes. Therefore, its elevated degree of phosphorylation may have an impact on these processes and, consequently, on the cortical development. Phospho-p38 and both total JNK and phospho-JNK, which regulate apoptosis, are reduced following undernutrition. However, cleaved caspase 3 is not altered, which suggests that this condition does not induce extensive modifications to the cortical apoptosis. Thus, our results indicate that undernutrition gives rise to molecular alterations that may have repercussions on cerebral cortex development and functions.

Topics: Age Factors; AMP-Activated Protein Kinases; Animals; Animals, Newborn; Animals, Suckling; Body Weight; Cerebral Cortex; Enzyme Activation; Female; Glycogen; Glycogen Synthase Kinase 3; JNK Mitogen-Activated Protein Kinases; Malnutrition; Organ Size; p38 Mitogen-Activated Protein Kinases; Pregnancy; Prenatal Nutritional Physiological Phenomena; Rats; Rats, Wistar

Topics: Glycogen; Glycogenolysis; Humans; Liver; Malnutrition; Metabolic Diseases; Nutrition Disorders; Nutritional Status

Topics: Glycogen; Humans; Liver Glycogen; Malnutrition