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Current Opinion in Clinical Nutrition... Jan 2009To draw attention to recent work on the role of protein and the amount of protein needed with each meal to preserve skeletal muscle mass in ageing. (Review)
Review
PURPOSE OF REVIEW
To draw attention to recent work on the role of protein and the amount of protein needed with each meal to preserve skeletal muscle mass in ageing.
RECENT FINDINGS
Ageing does not inevitably reduce the anabolic response to a high-quality protein meal. Ingestion of approximately 25-30 g of protein per meal maximally stimulates muscle protein synthesis in both young and older individuals. However, muscle protein synthesis is blunted in elderly when protein and carbohydrate are coingested or when the quantity of protein is less than approximately 20 g per meal. Supplementing regular mixed-nutrient meals with leucine may also enhance the muscle protein synthetic response in elders.
SUMMARY
On the basis of recent work, we propose a novel and specific dietary approach to prevent or slow down muscle loss with ageing. Rather than recommending a large, global increase in the recommended dietary allowance (RDA) for protein for all elderly individuals, clinicians should stress the importance of ingesting a sufficient amount of protein with each meal. To maximize muscle protein synthesis while being cognizant of total energy intake, we propose a dietary plan that includes 25-30 g of high quality protein per meal.
Topics: Aged; Aging; Dietary Proteins; Dietary Supplements; Exercise; Humans; Leucine; Muscle Proteins; Muscular Atrophy; Nutrition Policy; Protein Deficiency
PubMed: 19057193
DOI: 10.1097/MCO.0b013e32831cef8b -
The Indian Journal of Medical Research Nov 2009Oedematous malnutrition, represented by its most severe form kwashiorkor, is rampant in many parts of the world and is associated with a high case fatality rate. Despite... (Review)
Review
Oedematous malnutrition, represented by its most severe form kwashiorkor, is rampant in many parts of the world and is associated with a high case fatality rate. Despite being first described more than a century ago, the pathogenesis of kwashiorkor is still not clear. The traditional thinking is that it results from a deficiency of dietary protein and is usually associated with an infection. This has now been challenged by the finding that there is no difference in diets of children developing marasmus or kwashiorkor. Nutritional oedema is associated with an increased secretion of anti-diuretic substance (probably antidiuretic hormone) which prevents the normal excretory response to water administration. Experimental studies have shown that feeding low-protein, low-calorie diets results in delayed and incomplete response to a water load, and that the livers of the animals show a reduced capacity for inactivating anti-diuretic hormone. There is now evidence that links generation of free radicals and depletion of anti-oxidants with the development of oedema in kwashiorkor.
Topics: Aldosterone; Animals; Child; Edema; Ferritins; Humans; Kwashiorkor; Malnutrition; Models, Biological; Oxidative Stress; Protein-Energy Malnutrition; Vasopressins
PubMed: 20090122
DOI: No ID Found -
Annals of Nutrition & Metabolism 2016From the 1950s to the mid-1970s, United Nations (UN) agencies were focused on protein malnutrition as the major worldwide nutritional problem. The goal of this review is... (Review)
Review
BACKGROUND
From the 1950s to the mid-1970s, United Nations (UN) agencies were focused on protein malnutrition as the major worldwide nutritional problem. The goal of this review is to examine this era of protein malnutrition, the reasons for its demise, and the aftermath.
SUMMARY
The UN Protein Advisory Group was established in 1955. International conferences were largely concerned about protein malnutrition in children. By the early 1970s, UN agencies were ringing the alarm about a 'protein gap'. In The Lancet in 1974, Donald McLaren branded these efforts as 'The Great Protein Fiasco', declaring that the 'protein gap' was a fallacy. The following year, John Waterlow, the scientist who led most of the efforts on protein malnutrition, admitted that a 'protein gap' did not exist and that young children in developing countries only needed sufficient energy intake. The emphasis on protein malnutrition waned. It is recently apparent that quality protein and essential amino acids are missing in the diet and may have adverse consequences for child growth and the reduction of child stunting. Key Messages: It may be time to re-include protein and return protein malnutrition in the global health agenda using a balanced approach that includes all protective nutrients.
Topics: Adult; Amino Acids, Essential; Child; Child Nutritional Physiological Phenomena; Developing Countries; Diet, Healthy; Diet, Protein-Restricted; Female; Global Health; Health Transition; Humans; Infant; Kwashiorkor; Male; Malnutrition; Maternal Nutritional Physiological Phenomena; Nutritional Requirements; Pregnancy; Protein-Energy Malnutrition; United Nations
PubMed: 27576545
DOI: 10.1159/000449175 -
British Medical Journal Feb 1964
Topics: Adolescent; Blood Protein Disorders; Child; Chyle; Fistula; Humans; Hyperplasia; Hypertrophy; Lymphatic System; Lymphedema; Lymphography; Prognosis; Protein Deficiency; Surgical Procedures, Operative; Thoracic Duct
PubMed: 14101998
DOI: 10.1136/bmj.1.5382.529 -
Cell Death & Disease Oct 2022Acute pancreatitis is a common acute inflammatory abdominal disease. When acute pancreatitis progresses to severe acute pancreatitis (SAP), it can lead to systemic...
Acute pancreatitis is a common acute inflammatory abdominal disease. When acute pancreatitis progresses to severe acute pancreatitis (SAP), it can lead to systemic inflammation and even multiple organ failure. Thioredoxin-interacting protein (TXNIP) is an important protein involved in redox reactions of the inflammatory response. However, the specific role of TXNIP in SAP remains unclear. In this study, we investigated the role of thioredoxin interacting protein (TXNIP) in acute pancreatitis when induced by high doses of arginine. We found that pancreatic damage and the inflammatory response associated with acute pancreatitis were largely restrained in TXNIP knock-out mice but were enhanced in mice overexpressing TXNIP. Interestingly, the phosphorylation of p38, JNK, and ASK1 diminished in TXNIP-KO mice with pancreatitis in comparison with wild-type mice. The role of oxidative stress in SAP was explored in two models: TXNIP and AVV-TXNIP. TXNIP knockdown or the inhibition of ASK1 by gs-4997 abrogated the increase in p-p38, p-JNK, and p-ASK1 in AR42J cells incubated with L-Arg. The administration of gs-4997 to mice with pancreatitis largely reduced the upregulation of IL-6, IL-1β, TNF-α, and MCP-1. Systemic inflammatory reactions and injury in the lungs and kidneys were assessed in TXNIP-KO and AVV-TXNIP mice with expected outcomes. In conclusion, TXNIP is a novel mediator of SAP and exerts action by regulating inflammatory responses and oxidative stress via the ASK1-dependent activation of the JNK/p38 pathways. Thus, targeting TXNIP may represent a promising approach to protect against SAP.
Topics: Animals; Mice; Acute Disease; Apoptosis; MAP Kinase Kinase Kinase 5; Pancreatitis; Protein Deficiency; Thioredoxins
PubMed: 36316322
DOI: 10.1038/s41419-022-05355-x -
Advances in Nutrition (Bethesda, Md.) Jan 2011
Topics: Amino Acids; Amino Acids, Essential; Child, Preschool; Diet; Dietary Proteins; Female; Humans; Male; Nutrition Policy; Nutritional Requirements; Pregnancy; Protein Deficiency
PubMed: 22211190
DOI: 10.3945/an.110.000091 -
Cellular and Molecular Gastroenterology... 2021Chronic amino acid (AA) deficiency, as in kwashiorkor, reduces the size of the pancreas through an effect on mammalian target of rapamycin complex 1 (mTORC1). Because of...
BACKGROUND & AIMS
Chronic amino acid (AA) deficiency, as in kwashiorkor, reduces the size of the pancreas through an effect on mammalian target of rapamycin complex 1 (mTORC1). Because of the physiological importance of AAs and their role as a substrate, a stimulant of mTORC1, and protein synthesis, we studied the effect of acute protein and AA deficiency on the response to feeding.
METHODS
ICR/CD-1 mice were fasted overnight and refed for 2 hours with 4 different isocaloric diets: control (20% Prot); Protein-free (0% Prot); control (AA-based diet), and a leucine-free (No Leu). Protein synthesis, polysomal profiling, and the activation of several protein translation factors were analyzed in pancreas samples.
RESULTS
All diets stimulated the Protein Kinase-B (Akt)/mTORC1 pathway, increasing the phosphorylation of the kinase Akt, the ribosomal protein S6 (S6) and the formation of the eukaryotic initiation factor 4F (eIF4F) complex. Total protein synthesis and polysome formation were inhibited in the 0% Prot and No Leu groups to a similar extent, compared with the 20% Prot group. The 0% Prot diet partially reduced the Akt/mTORC1 pathway and the activity of the guanine nucleotide exchange factor eIF2B, without affecting eIF2α phosphorylation. The No Leu diet increased the phosphorylation of eIF2α and general control nonderepressible 2, and also inhibited eIF2B activity, without affecting mTORC1. Essential and nonessential AA levels in plasma and pancreas indicated a complex regulation of their cellular transport mechanisms and their specific effect on the synthesis of digestive enzymes.
CONCLUSIONS
These studies show that dietary AAs are important regulators of postprandial digestive enzyme synthesis, and their deficiency could induce pancreatic insufficiency and malnutrition.
Topics: Animals; Diet, Protein-Restricted; Disease Models, Animal; Eukaryotic Initiation Factor-2; Exocrine Pancreatic Insufficiency; Humans; Leucine; Male; Mechanistic Target of Rapamycin Complex 1; Mice; Pancreas; Phosphorylation; Postprandial Period; Protein Biosynthesis; Protein Deficiency
PubMed: 32735995
DOI: 10.1016/j.jcmgh.2020.07.008 -
Scientific Reports Jun 2021To study, in young growing rats, the consequences of different levels of dietary protein deficiency on food intake, body weight, body composition, and energy balance and...
To study, in young growing rats, the consequences of different levels of dietary protein deficiency on food intake, body weight, body composition, and energy balance and to assess the role of FGF21 in the adaptation to a low protein diet. Thirty-six weanling rats were fed diets containing 3%, 5%, 8%, 12%, 15% and 20% protein for three weeks. Body weight, food intake, energy expenditure and metabolic parameters were followed throughout this period. The very low-protein diets (3% and 5%) induced a large decrease in body weight gain and an increase in energy intake relative to body mass. No gain in fat mass was observed because energy expenditure increased in proportion to energy intake. As expected, Fgf21 expression in the liver and plasma FGF21 increased with low-protein diets, but Fgf21 expression in the hypothalamus decreased. Under low protein diets (3% and 5%), the increase in liver Fgf21 and the decrease of Fgf21 in the hypothalamus induced an increase in energy expenditure and the decrease in the satiety signal responsible for hyperphagia. Our results highlight that when dietary protein decreases below 8%, the liver detects the low protein diet and responds by activating synthesis and secretion of FGF21 in order to activate an endocrine signal that induces metabolic adaptation. The hypothalamus, in comparison, responds to protein deficiency when dietary protein decreases below 5%.
Topics: Animals; Diet, Protein-Restricted; Disease Models, Animal; Energy Intake; Energy Metabolism; Fibroblast Growth Factors; Humans; Hypothalamus; Liver; Male; Protein Deficiency; Rats; Satiety Response
PubMed: 34127689
DOI: 10.1038/s41598-021-91274-4 -
Glia Jul 2022Survival motor neuron (SMN) protein deficiency results in loss of alpha motor neurons and subsequent muscle atrophy in patients with spinal muscular atrophy (SMA)....
Survival motor neuron (SMN) protein deficiency results in loss of alpha motor neurons and subsequent muscle atrophy in patients with spinal muscular atrophy (SMA). Reactive microglia have been reported in SMA mice and depleting microglia rescues the number of proprioceptive synapses, suggesting a role in SMA pathology. Here, we explore the contribution of lymphocytes on microglia reactivity in SMA mice and investigate how SMN deficiency alters the reactive profile of human induced pluripotent stem cell (iPSC)-derived microglia. We show that microglia adopt a reactive morphology in spinal cords of SMA mice. Ablating lymphocytes did not alter the reactive morphology of SMA microglia and did not improve the survival or motor function of SMA mice, indicating limited impact of peripheral immune cells on the SMA phenotype. We found iPSC-derived SMA microglia adopted an amoeboid morphology and displayed a reactive transcriptome profile, increased cell migration, and enhanced phagocytic activity. Importantly, cell morphology and electrophysiological properties of motor neurons were altered when they were incubated with conditioned media from SMA microglia. Together, these data reveal that SMN-deficient microglia adopt a reactive profile and exhibit an exaggerated inflammatory response with potential impact on SMA neuropathology.
Topics: Animals; Disease Models, Animal; Humans; Induced Pluripotent Stem Cells; Mice; Microglia; Motor Neurons; Muscular Atrophy, Spinal; Protein Deficiency; Survival of Motor Neuron 1 Protein
PubMed: 35373853
DOI: 10.1002/glia.24177 -
Nutrients Apr 2019Skeletal muscle (SM) mass, the chief component of the structural compartment belonging to lean body mass (LBM), undergoes sarcopenia with increasing age. Decreased SM in... (Review)
Review
Skeletal muscle (SM) mass, the chief component of the structural compartment belonging to lean body mass (LBM), undergoes sarcopenia with increasing age. Decreased SM in elderly persons is a naturally occurring process that may be accelerated by acute or chronic nutritional deficiencies and/or inflammatory disorders, declining processes associated with harmful complications. A recently published position paper by European experts has provided an overall survey on the definition and diagnosis of sarcopenia in elderly persons. The present review describes the additional contributory role played by the noninvasive transthyretin (TTR) micromethod. The body mass index (BMI) formula is currently used in clinical studies as a criterion of good health to detect, prevent, and follow up on the downward trend of muscle mass. The recent upsurge of sarcopenic obesity with its multiple subclasses has led to a confused stratification of SM and fat stores, prompting workers to eliminate BMI from screening programs. As a result, investigators are now focusing on indices of protein status that participate in SM growth, maturation, and catabolism that might serve to identify sarcopenia trajectories. Plasma TTR is clearly superior to all other hepatic biomarkers, showing the same evolutionary patterns as those displayed in health and disease by both visceral and structural LBM compartments. As a result, this TTR parameter maintains positive correlations with muscle mass downsizing in elderly persons. The liver synthesis of TTR is downregulated in protein-depleted states and suppressed in cytokine-induced inflammatory disorders. TTR integrates the centrally-mediated regulatory mechanisms governing the balance between protein accretion and protein breakdown, emerging as the ultimate indicator of LBM resources. This review proposes the adoption of a gray zone defined by cut-off values ranging from 200 mg/L to 100 mg/L between which TTR plasma values may fluctuate and predict either the best or the worst outcome. The best outcome occurs when appropriate dietary, medicinal and surgical decisions are undertaken, resuming TTR synthesis which manifests rising trends towards pre-stress levels. The worst occurs when all therapeutic means fail to succeed, leading inevitably to complete exhaustion of LBM and SM metabolic resources with an ensuing fatal outcome. Some patients may remain unresponsive in the middle of the gray area, combining steady clinical states with persistent stagnant TTR values. Using the serial measurement of plasma TTR values, these last patients should be treated with the most aggressive and appropriate therapeutic strategies to ensure the best outcome.
Topics: Adipose Tissue; Aged; Biomarkers; Body Composition; Body Fluid Compartments; Body Mass Index; Humans; Inflammation; Liver; Muscle, Skeletal; Nutritional Status; Obesity; Prealbumin; Protein Deficiency; Sarcopenia
PubMed: 31010086
DOI: 10.3390/nu11040895