Glucose, Lipid, and Protein Metabolism

2011 ◽  
Author(s):  
Gregory O. Clark ◽  
William J. Kovacs
Keyword(s):  
Adipose Tissue ◽  
Protein Metabolism ◽  
Caloric Intake ◽  
Acid Synthesis ◽  
Food Ingestion ◽  
Complex Energy ◽  
Biochemical Processes ◽  
The Individual ◽  
Amino Acid Concentrations ◽  
Feeding And Fasting

The maintenance of life requires a constant supply of substrate for the generation of energy and preservation of the structure of cells and tissues. The process in principle is simple, yet the individual metabolic pathways and the regulation of substrate fluxes through these pathways can be complex. Energy is derived when fuel substrates are oxidized to carbon dioxide and water in the presence of oxygen, generating adenosine triphosphate (ATP). A portion of the ingested foodstuff is also utilized, either directly or after transformation into other substrates, to repair and replace cell membranes, structural proteins, and organelles. The remainder is stored as potential energy in the form of glycogen or fat. Under normal circumstances, each individual remains in a near-steady state where weight and appearance are stable over prolonged periods. In the short term, fuel metabolism changes dramatically several times a day during alternating periods of feeding and fasting. An anabolic phase begins with food ingestion and lasts for several hours. Energy storage occurs during this period when caloric intake exceeds caloric demands. The catabolic phase usually begins 4 to 6 hours after a meal and lasts until the person eats once again. During this phase, utilization shifts from exogenous to endogenous fuels, a change heralded by the mobilization of substrate stored in liver, muscle, and adipose tissue. Both anabolic and catabolic phases are characterized by specific biochemical processes regulated by distinct hormonal profiles. In the anabolic phase that follows ingestion of a mixed meal, substrate flux is directed from the intestine through the liver to storage and utilization sites. Glucose, triglyceride, and amino acid concentrations increase in plasma, whereas those of fatty acids, ketones (acetoacetic and β -hydroxy-butyric acids), and glycerol decrease. Both glycogen and protein synthesis begin in liver and muscle, while fatty acid synthesis and triglyceride esterification are stimulated in hepatocytes and adipose tissue. In the catabolic phase, the biochemical activities are reversed and the flux of fuel is directed from storage depots to liver and other utilization sites.

Specialized Diet Therapies: Exploration for Improving Behavior in Autism Spectrum Disorder (ASD)

2020 ◽  
Vol 27 (40) ◽  
pp. 6771-6786
Author(s):  
Geir Bjørklund ◽  
Nagwa Abdel Meguid ◽  
Maryam Dadar ◽  
Lyudmila Pivina ◽  
Joanna Kałużna-Czaplińska ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Neurodevelopmental Disorder ◽  
Caloric Intake ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Nutritional Deficiencies ◽  
Childhood And Adolescence ◽  
Restricted Interests ◽  
Balanced Diet ◽  
The Individual

As a major neurodevelopmental disorder, Autism Spectrum Disorder (ASD) encompasses deficits in communication and repetitive and restricted interests or behaviors in childhood and adolescence. Its etiology may come from either a genetic, epigenetic, neurological, hormonal, or an environmental cause, generating pathways that often altogether play a synergistic role in the development of ASD pathogenesis. Furthermore, the metabolic origin of ASD should be important as well. A balanced diet consisting of the essential and special nutrients, alongside the recommended caloric intake, is highly recommended to promote growth and development that withstand the physiologic and behavioral challenges experienced by ASD children. In this review paper, we evaluated many studies that show a relationship between ASD and diet to develop a better understanding of the specific effects of the overall diet and the individual nutrients required for this population. This review will add a comprehensive update of knowledge in the field and shed light on the possible nutritional deficiencies, metabolic impairments (particularly in the gut microbiome), and malnutrition in individuals with ASD, which should be recognized in order to maintain the improved socio-behavioral habit and physical health.

scholarly journals Effects of Prolactin in Vitro on Fatty Acid Synthesis in Rat Adipose Tissue

1959 ◽  
Vol 234 (12) ◽  
pp. 3111-3114 ◽  
Author(s):  
Albert I. Winegrad ◽  
Walter N. Shaw ◽  
Francis D.W. Lukens ◽  
William C. Stadie
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Rat Adipose Tissue

Effect of carbohydrate intake on de novo lipogenesis in human adipose tissue

1987 ◽  
Vol 253 (6) ◽  
pp. E664-E669 ◽  
Author(s):  
C. Chascione ◽  
D. H. Elwyn ◽  
M. Davila ◽  
K. M. Gil ◽  
J. Askanazi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
De Novo ◽  
Acid Synthesis ◽  
De Novo Lipogenesis ◽  
Whole Body ◽  
High Intake ◽  
Carbohydrate Diet ◽  
Triglyceride Synthesis ◽  
High Carbohydrate

Rates of synthesis, from [14C]glucose, of fatty acids (de novo lipogenesis) and glycerol (triglyceride synthesis) were measured in biopsies of adipose tissue from nutritionally depleted patients given low- or high-carbohydrate intravenous nutrition. Simultaneously, energy expenditure and whole-body lipogenesis were measured by indirect calorimetry. Rates of whole-body lipogenesis were zero on the low-carbohydrate diet and averaged 1.6 g.kg-1.day-1 on the high-carbohydrate diet. In vitro rates of triglyceride synthesis increased 3-fold going from the low to the high intake; rates of fatty acid synthesis increased approximately 80-fold. In vitro, lipogenesis accounted for less than 0.1% of triglyceride synthesis on the low intake and 4% on the high intake. On the high-carbohydrate intake, in vitro rates of triglyceride synthesis accounted for 61% of the rates of unidirectional triglyceride synthesis measured by indirect calorimetry. In vitro rates of lipogenesis accounted for 7% of whole-body lipogenesis. Discrepancies between in vitro rates of fatty acid synthesis from glucose, compared with acetate and citrate, as reported by others, suggest that in depleted patients on hypercaloric high-carbohydrate diets, adipose tissue may account for up to 40% of whole-body lipogenesis.

Low-protein, high-carbohydrate diet increases glucose uptake and fatty acid synthesis in brown adipose tissue of rats

Nutrition ◽  
2014 ◽  
Vol 30 (4) ◽  
pp. 473-480 ◽  
Author(s):  
Suélem Aparecida de França ◽  
Maísa Pavani dos Santos ◽  
Roger Vinícius Nunes Queiroz da Costa ◽  
Mendalli Froelich ◽  
Samyra Lopes Buzelle ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Low Protein ◽  
Brown Adipose

scholarly journals Regulation of fatty acid synthesis and malonyl-CoA content in mouse brown adipose tissue in response to cold-exposure, starvation or re-feeding

1987 ◽  
Vol 243 (2) ◽  
pp. 437-442 ◽  
Author(s):  
M G Buckley ◽  
E A Rath
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
Cold Exposure ◽  
Acid Synthesis ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Malonyl Coa ◽  
Brown Adipose

1. The effect of nutritional status on fatty acid synthesis in brown adipose tissue was compared with the effect of cold-exposure. Fatty acid synthesis was measured in vivo by 3H2O incorporation into tissue lipids. The activities of acetyl-CoA carboxylase and fatty acid synthetase and the tissue concentrations of malonyl-CoA and citrate were assayed. 2. In brown adipose tissue of control mice, the tissue content of malonyl-CoA was 13 nmol/g wet wt., higher than values reported in other tissues. From the total tissue water content, the minimum possible concentration was estimated to be 30 microM 3. There were parallel changes in fatty acid synthesis, malonyl-CoA content and acetyl-CoA carboxylase activity in response to starvation and re-feeding. 4. There was no correlation between measured rates of fatty acid synthesis and malonyl-CoA content and acetyl-CoA carboxylase activity in acute cold-exposure. The results suggest there is simultaneous fatty acid synthesis and oxidation in brown adipose tissue of cold-exposed mice. This is probably effected not by decreases in the malonyl-CoA content, but by increases in the concentration of free long-chain fatty acyl-CoA or enhanced peroxisomal oxidation, allowing shorter-chain fatty acids to enter the mitochondria independent of carnitine acyltransferase (overt form) activity.

Effect of Cytokinins on the Expansion and Metabolism of Excised Cucumber Cotyledons

1980 ◽  
Vol 7 (3) ◽  
pp. 227
Author(s):  
C Tsui ◽  
Tao Guo-qing ◽  
Chen Hui-ying ◽  
Son Yan-ru ◽  
Lian Han-ping ◽  
...  
Keyword(s):  
Nucleic Acid ◽  
Soluble Sugars ◽  
Dry Weight ◽  
Acid Synthesis ◽  
Cell Number ◽  
Cucumis Sativus L ◽  
Biochemical Processes ◽  
Dna And Rna ◽  
Lag Period ◽  
Hydrolysis Of

Expansion of excised cucumber (Cucumis sativus L.) cotyledons was stimulated by treatment with cytokinin, and commenced after a lag period of about 4 h. Expansion induced by benzyladenine (BA) was due mainly to increase of fresh weight, but cell number increased slightly. Hydrolysis of protein and lipid was stimulated by BA, and soluble sugars increased simultaneously. However, there was no significant change in the dry weight of cotyledons during the period of expansion. It is assumed that the transformation of lipid to sugar in the cotyledon is stimulated by BA. The respiration of cotyledons was evidently stimulated by BA and was entirely inhibited by respiratory inhibitors, e.g. NaN,, malonate and dinitrophenol. Inhibitors of protein and nucleic acid synthesis, such as chloramphenicol and actinomycin D, inhibited only the BA-induced expansion. They had no effect on the expansion of controls. These results suggest that different biochemical processes are involved in the expansion of cotyledons induced by BA and in controls. The former is related not only to respiration but also to the synthesis of protein and nucleic acid. BA increased DNA and RNA content per cotyledon. The increase of total RNA is due mainly to the increase of 25 S and 18 S rRNA.

Metabolic fuel homeostasis in golden hamsters: effects of fasting, refeeding, glucose, and insulin

1984 ◽  
Vol 247 (1) ◽  
pp. R57-R62 ◽  
Author(s):  
N. Rowland
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Acid Synthesis ◽  
Ingestive Behavior ◽  
Metabolic Responses ◽  
Exogenous Insulin ◽  
Rapid Reversal

Experiments were conducted to investigate possible metabolic correlates of the unusual ingestive behavior of hamsters after food deprivation. A hypothesis of metabolic refractoriness predicts that hamsters, unlike rats, should not show changes in plasma metabolic fuels, adipose tissue, or liver after fasting and subsequent refeeding. This hypothesis was discredited by findings that fasted hamsters, like rats, have increased plasma ketones and free fatty acids and decreased liver glycogen. On refeeding, hamsters showed rapid reversal of these changes, with supranormal glycogen content and apparent fatty acid synthesis in liver. Additional studies examined the metabolic responses of hamsters and rats to exogenous insulin or glucose administration. Incorporation of 3H2O into liver fatty acids was greatly elevated in rats by both insulin and glucose, but in hamsters only insulin was effective. Some of these metabolic differences may help our understanding of the unusual refractoriness of hamster food intake to various stimuli.

scholarly journals Modeling the Effect of High Calorie Diet on the Interplay between Adipose Tissue, Inflammation, and Diabetes

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
V. Prana ◽  
P. Tieri ◽  
M.C. Palumbo ◽  
E. Mancini ◽  
F. Castiglione
Keyword(s):  
Adipose Tissue ◽  
Chronic Inflammation ◽  
Blood Glucose Concentration ◽  
Caloric Intake ◽  
Direct Consequence ◽  
Calorie Intake ◽  
Human Organism ◽  
Inflammatory State ◽  
Set Up ◽  
High Calorie

Background. Type 2 diabetes (T2D) is a chronic metabolic disease potentially leading to serious widespread tissue damage. Human organism develops T2D when the glucose-insulin control is broken for reasons that are not fully understood but have been demonstrated to be linked to the emergence of a chronic inflammation. Indeed such low-level chronic inflammation affects the pancreatic production of insulin and triggers the development of insulin resistance, eventually leading to an impaired control of the blood glucose concentration. On the contrary, it is well-known that obesity and inflammation are strongly correlated. Aim. In this study, we investigate in silico the effect of overfeeding on the adipose tissue and the consequent set up of an inflammatory state. We model the emergence of the inflammation as the result of adipose mass increase which, in turn, is a direct consequence of a prolonged excess of high calorie intake. Results. The model reproduces the fat accumulation due to excessive caloric intake observed in two clinical studies. Moreover, while showing consistent weight gains over long periods of time, it reveals a drift of the macrophage population toward the proinflammatory phenotype, thus confirming its association with fatness.

Sign in / Sign up

Export Citation Format

Share Document