scholarly journals Increased Diurnal Activity Is Indicative of Energy Deficit in a Nocturnal Mammal, the Aardvark

2020 ◽  
Vol 11 ◽  
Author(s):  
Nora Marie Weyer ◽  
Andrea Fuller ◽  
Anna Jean Haw ◽  
Leith Carl Rodney Meyer ◽  
Duncan Mitchell ◽  
...  
Keyword(s):  
Energy Deficit ◽  
Diurnal Activity ◽  
Nocturnal Mammal

Adolescent athletes and nutrition – analysis of two groups of children

2020 ◽  
pp. 1-6
Author(s):  
Tatyana Dzimbova
Keyword(s):  
Energy Expenditure ◽  
Energy Intake ◽  
Eating Habits ◽  
Energy Deficit ◽  
Young Athletes ◽  
Adolescent Athletes ◽  
Basketball Players ◽  
Calcium Magnesium ◽  
The Right

Introduction. Proper nutrition is crucial for child and adolescent athletes to maintain growth and development and to achieveoptimal results in sports. It is very important to balance the energy expenditure with the energy intake in order to prevent the energy deficit or excess.Materials and methods. Subjects involved in two different sports participated in the study: 13 gymnasts (age 13.8 ± 4.1 years, height 153.4 ± 11.3 cm, weight 47.1 ± 10.5 kg) and 15 basketball players (age 15.5 ± 1.1 years, height 176.7 ± 7.9 cm, weight 65.2 ± 10.7 kg). Determination of total energy expenditure was made by prediction equations. The subjects maintained a food records for 5 consecutive days, which were processed in the ASA24 system of the NCI. Results and discussion. Energy intake in both groups is sufficient to meet the daily needs, development of young athletes andprovide the energy needed in training. The intake of three minerals (calcium, magnesium and potassium) and three vitamins (D, E and A) was lower than recommended values in both groups.Conclusion. As a result of the busy schedule of adolescent athletes, their main meals are out of home, and the proportion of highly processed foods containing small amounts of important vitamins and minerals is high. The main recommendations include dairy products, fruits, vegetables and whole grains. The idea behind the changes is to give young athletes the right diet and the right eating habits.

23 Nutritional Intake and Weight Change in Severely Burned Patients

2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S20-S21
Author(s):  
Sandrine O Fossati ◽  
Beth A Shields ◽  
Renee E Cole ◽  
Adam J Kieffer ◽  
Saul J Vega ◽  
...  
Keyword(s):  
Wound Healing ◽  
Mass Loss ◽  
Performance Improvement ◽  
Body Mass ◽  
Total Body Surface Area ◽  
Nutritional Intake ◽  
Energy Deficit ◽  
Body Mass Loss ◽  
Improvement Project ◽  
Burn Care

Abstract Introduction Nutrition is crucial for recovery from burn injuries, as severe weight (wt.) loss can lead to impaired immunity and wound healing, infections, skin graft failure, and mortality. Previous studies recommended avoiding more than 10% wt. loss, as this level resulted in increased infection rates. However, wt. loss is often not quantifiable during the critical illness phase, with severe edema masking non-fluid related body wt. changes. Energy (kcal) deficits can be used to estimate wt. loss until the edema has resolved, but previous studies in non-burn patients indicate that actual wt. loss is less than the commonly used 3500 kcal per pound of fat (7700 kcal per kg of fat). The objective of this performance improvement project was to evaluate nutritional intake and the resulting dry wt. change in severely burned patients. Methods This performance improvement project was approved by our regulatory compliance division. We performed a retrospective evaluation on patients with at least 20% total body surface area (TBSA) burns admitted for initial burn care to our intensive care unit over a 7-year period. Patients who died or who had major fascial excisions or limb amputations were excluded. Patients who did not achieve a recorded dry wt. after wound healing were not included in this analysis. Retrospective data were collected, including sex, age, burn size, kcal intake, kcal goal per the Milner equation using activity factor of 1.4, admission dry wt., dry wt. after wound healing (defined as less than 10% TBSA open wound), and days to dry wt. after wound healing. Descriptive statistics and linear regression were performed using JMP. Significance was set at p< 0.05. Results The 30 included patients had the following characteristics: 90% male, 30 ± 11 years old, 45% ± 15% TBSA burn. They received 2720 ± 1092 kcal/day, meeting 68% ± 24% kcal goal, and took approximately 53 ± 30 days from injury to achieve dry wt. after wound healing. These patients had wt. loss of 8 ± 8 kg from the kcal deficit of 69,819 ± 51,704 during this time period. The kcal deficit was significantly associated with wt. change [p < 0.001, R2 = 0.49, wt. change in kg = (-0.000103 x kcal deficit) – 1]. This translates to one kg of body wt. loss resulting from 9709 kcal deficit. Conclusions This performance improvement project found that an energy deficit of approximately 9700 kcal in our patients equates to 1 kg of body mass loss (4400 kcal deficit equates to 1 pound of body mass loss). These findings are similar to wt. loss studies in other patient populations and contrary to the commonly used 3500 kcal per pound of fat (7700 kcal per kg of fat).

scholarly journals Generation and Evaluation of Isogenic iPSC as a Source of Cell Replacement Therapies in Patients with Kearns Sayre Syndrome

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 568
Author(s):  
Glen Lester Sequiera ◽  
Abhay Srivastava ◽  
Keshav Narayan Alagarsamy ◽  
Cheryl Rockman-Greenberg ◽  
Sanjiv Dhingra
Keyword(s):  
Mononuclear Cells ◽  
Therapeutic Option ◽  
Reactive Oxygen Species Generation ◽  
Energy Deficit ◽  
Patient Specific ◽  
Multisystem Disorder ◽  
Differentiation Potential ◽  
Cell Replacement ◽  
Mtdna Mutations ◽  
Kearns Sayre Syndrome

Kearns Sayre syndrome (KSS) is mitochondrial multisystem disorder with no proven effective treatment. The underlying cause for multisystem involvement is the energy deficit resulting from the load of mutant mitochondrial DNA (mtDNA), which manifests as loss of cells and tissue dysfunction. Therefore, functional organ or cellular replacement provides a promising avenue as a therapeutic option. Patient-specific induced pluripotent stem cells (iPSC) have become a handy tool to create personalized cell -based therapies. iPSC are capable of self-renewal, differentiation into all types of body cells including cardiomyocytes (CM) and neural progenitor cells (NPC). In KSS patients, mutations in mtDNA are largely found in the muscle tissue and are predominantly absent in the blood cells. Therefore, we conceptualized that peripheral blood mononuclear cells (PBMNC) from KSS patients can be reprogrammed to generate mutation free, patient specific iPSC lines that can be used as isogenic source of cell replacement therapies to treat affected organs. In the current study we generated iPSC lines from two female patients with clinical diagnosis of classic KSS. Our data demonstrate that iPSC from these KSS patients showed normal differentiation potential toward CM, NPC and fibroblasts without any mtDNA deletions over passages. Next, we also found that functional studies including ATP production, reactive oxygen species generation, lactate accumulation and mitochondrial membrane potential in iPSC, CM, NPC and fibroblasts of these KSS patients were not different from respective cells from healthy controls. PBMNCs from these KSS patients in the current study did not reproduce mtDNA mutations which were present in muscle biopsies. Furthermore, we demonstrate for the first time that this phenomenon provides opportunities to create isogenic mutation free iPSC with absent or very low level of expression of mtDNA deletion which can be banked for future cell replacement therapies in these patients as the disease progresses.

Energy Intakes of Ultraendurance Cyclists During Competition, an Observational Study

2012 ◽  
Vol 22 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Katherine E. Black ◽  
Paula M.L. Skidmore ◽  
Rachel C. Brown
Keyword(s):  
Observational Study ◽  
Energy Intake ◽  
Energy Requirement ◽  
Negative Relationship ◽  
Computer Software ◽  
High Energy ◽  
Energy Deficit ◽  
Food Diary ◽  
Food And Drink ◽  
And Performance

Endurance events >10 hr are becoming increasingly popular but provide numerous physiological challenges, several of which can be attenuated with optimal nutritional intakes. Previous studies in ultraendurance races have reported large energy deficits during events. The authors therefore aimed to assess nutritional intakes in relation to performance among ultraendurance cyclists. This observational study included 18 cyclists in a 384-km cycle race. At race registration each cyclist’s support crew was provided with a food diary for their cyclist. On completion of the race, cyclists were asked to recall their race food and drink intakes. All food and fluids were analyzed using a computer software package. Mean (SD) time to complete the race was 16 hr 21 min (2 hr 2 min). Mean (SD) energy intake was 18.7 (8.6) MJ, compared with an estimated energy requirement for the race of 25.5 (7.4) MJ. There was a significant negative relationship between energy intake and time taken to complete the race (p = .023, r2 = −.283). Mean (SD) carbohydrate, fat, and protein intakes were 52 (27), 15.84 (56.43), and 2.94 (7.25) g/hr, respectively. Only carbohydrate (p = .015, r2 = −.563) and fat intake (p = .037, r2 = −.494) were associated with time taken to complete the race. This study demonstrates the difficulties in meeting the high energy demands of ultraendurance cycling. The relationship between energy intake and performance suggests that reducing the energy deficit may be advantageous. Given the high carbohydrate intakes of these athletes, increasing energy intake from fat should be investigated as a means of decreasing energy deficits.

Relationship between Visceral Fat and PAI-1 in Overweight Men and Women before and after Weight Loss

1999 ◽  
Vol 82 (11) ◽  
pp. 1490-1496 ◽  
Author(s):  
M. Kockx ◽  
R. Leenen ◽  
J. Seidell ◽  
H. M. G. Princen ◽  
T. Kooistra
Keyword(s):  
Weight Loss ◽  
Fat Mass ◽  
Visceral Fat ◽  
Linear Regression Analysis ◽  
Energy Deficit ◽  
Obese Women ◽  
Plasminogen Activator Inhibitor 1 ◽  
Men And Women ◽  
Total Fat ◽  
Pai 1

SummaryThis study was aimed at evaluating the relationship between visceral fat accumulation and plasma plasminogen activator inhibitor-1 (PAI-1) levels in healthy, obese men and women undergoing weight loss therapy. The subjects, 25 men and 25 premenopausal women, aged between 26 and 49 years, with an initial body mass index between 28 and 38 kg/m2, received a controlled diet for 13 weeks providing a 4.2 MJ/day energy deficit. Magnetic resonance imaging was used to measure visceral and subcutaneous abdominal fat. Our results show that before weight loss visceral fat was significantly correlated with PAI-1 in men (r = 0.45; p <0.05), but not in women (r = -0.15; ns). The association between visceral fat and PAI-1 in men remained significant after adjustment for age and total fat mass, and multiple linear regression analysis showed a significant independent contribution of visceral fat to plasma PAI-1 levels. Both visceral fat areas and PAI-1 levels decreased significantly with weight loss in both men and women. Changes in visceral fat area were related to changes in PAI-1 in women (r = -0.43; p = 0.05) but not in men (r = -0.01; ns); however, this association in women disappeared after adjustment for total fat mass. We conclude that there is a relationship between visceral fat and PAI-1 in obese men but not in obese women, and that PAI-1 levels decrease substantially (52%) by weight loss, but this change is not related to changes in visceral fat mass per se.

scholarly journals Epilepsy in Mitochondrial Diseases—Current State of Knowledge on Aetiology and Treatment

Children ◽  
2021 ◽  
Vol 8 (7) ◽  
pp. 532
Author(s):  
Dorota Wesół-Kucharska ◽  
Dariusz Rokicki ◽  
Aleksandra Jezela-Stanek
Keyword(s):  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Disease ◽  
Clinical Picture ◽  
Poor Prognosis ◽  
Treatment Options ◽  
Mitochondrial Diseases ◽  
Energy Deficit ◽  
Atp Production ◽  
Current State

Mitochondrial diseases are a heterogeneous group of diseases resulting from energy deficit and reduced adenosine triphosphate (ATP) production due to impaired oxidative phosphorylation. The manifestation of mitochondrial disease is usually multi-organ. Epilepsy is one of the most common manifestations of diseases resulting from mitochondrial dysfunction, especially in children. The onset of epilepsy is associated with poor prognosis, while its treatment is very challenging, which further adversely affects the course of these disorders. Fortunately, our knowledge of mitochondrial diseases is still growing, which gives hope for patients to improve their condition in the future. The paper presents the pathophysiology, clinical picture and treatment options for epilepsy in patients with mitochondrial disease.

scholarly journals Oligodendroglial Energy Metabolism and (re)Myelination

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 238
Author(s):  
Vanja Tepavčević
Keyword(s):  
Energy Metabolism ◽  
Alternative Energy ◽  
Energy Homeostasis ◽  
Energy Deficit ◽  
Maturation Stage ◽  
Trophic Support ◽  
Important Contributor ◽  
Alternative Energy Sources ◽  
Axonal Pathology ◽  
Sufficient Energy

Central nervous system (CNS) myelin has a crucial role in accelerating the propagation of action potentials and providing trophic support to the axons. Defective myelination and lack of myelin regeneration following demyelination can both lead to axonal pathology and neurodegeneration. Energy deficit has been evoked as an important contributor to various CNS disorders, including multiple sclerosis (MS). Thus, dysregulation of energy homeostasis in oligodendroglia may be an important contributor to myelin dysfunction and lack of repair observed in the disease. This article will focus on energy metabolism pathways in oligodendroglial cells and highlight differences dependent on the maturation stage of the cell. In addition, it will emphasize that the use of alternative energy sources by oligodendroglia may be required to save glucose for functions that cannot be fulfilled by other metabolites, thus ensuring sufficient energy input for both myelin synthesis and trophic support to the axons. Finally, it will point out that neuropathological findings in a subtype of MS lesions likely reflect defective oligodendroglial energy homeostasis in the disease.

scholarly journals Mitochondrial Dysfunction in Atrial Fibrillation—Mechanisms and Pharmacological Interventions

2021 ◽  
Vol 10 (11) ◽  
pp. 2385
Author(s):  
Paweł Muszyński ◽  
Tomasz A. Bonda
Keyword(s):  
Atrial Fibrillation ◽  
Mitochondrial Dysfunction ◽  
Treatment Options ◽  
Therapeutic Interventions ◽  
Energy Deficit ◽  
Functional Changes ◽  
Electrical Instability ◽  
Ionic Fluxes ◽  
Prevention Methods ◽  
Invasive Techniques

Despite the enormous progress in the treatment of atrial fibrillation, mainly with the use of invasive techniques, many questions remain unanswered regarding the pathomechanism of the arrhythmia and its prevention methods. The development of atrial fibrillation requires functional changes in the myocardium that result from disturbed ionic fluxes and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying the arrhythmia may result from a cellular energy deficit and oxidative stress, which are caused by mitochondrial dysfunction. The significance of mitochondrial dysfunction in the pathogenesis of atrial fibrillation remains not fully elucidated; however, it is emphasized by the reduction of atrial fibrillation burden after therapeutic interventions improving the mitochondrial welfare. This review summarizes the mechanisms of mitochondrial dysfunction related to atrial fibrillation and current pharmacological treatment options targeting mitochondria to prevent or improve the outcome of atrial fibrillation.

scholarly journals Skeletal Muscle Metabolism: Origin or Prognostic Factor for Amyotrophic Lateral Sclerosis (ALS) Development?

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1449
Author(s):  
Cyril Quessada ◽  
Alexandra Bouscary ◽  
Frédérique René ◽  
Cristiana Valle ◽  
Alberto Ferri ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Muscle Metabolism ◽  
The Body ◽  
Energy Deficit ◽  
Acid Oxidation ◽  
Progression Of Disease ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive and selective loss of motor neurons, amyotrophy and skeletal muscle paralysis usually leading to death due to respiratory failure. While generally considered an intrinsic motor neuron disease, data obtained in recent years, including our own, suggest that motor neuron protection is not sufficient to counter the disease. The dismantling of the neuromuscular junction is closely linked to chronic energy deficit found throughout the body. Metabolic (hypermetabolism and dyslipidemia) and mitochondrial alterations described in patients and murine models of ALS are associated with the development and progression of disease pathology and they appear long before motor neurons die. It is clear that these metabolic changes participate in the pathology of the disease. In this review, we summarize these changes seen throughout the course of the disease, and the subsequent impact of glucose–fatty acid oxidation imbalance on disease progression. We also highlight studies that show that correcting this loss of metabolic flexibility should now be considered a major goal for the treatment of ALS.

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