Carbohydrate metabolism in adipose tissue -
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Topic: Hormonal Regulation And Integration Of Metabolism. It includes the following processes: Glycogenesis is the synthesis of glycogen from glucose. Glycogenolysis is the breakdown of glycogen to glucose. Gluconeogenesis is the synthesis of glucose from non-carbohydrate sources.
Lipid metabolism synthesizes and degrades lipid cells. It involves the following processes: Ketogenesis is the production of ketone bodies from acetyl-CoA in the absence of insulin. Beta-oxidation is the breakdown of fatty acids to generate acetyl-CoA.
Pentose phosphate pathway is the lipid and ribose synthesis. Conversion of excess carbohydrates and proteins into fatty acids for storage Protein metabolism is the synthesis and breakdown of proteins and amino acids.
It includes Deamination of amino acids for synthesis of glucose or lipids. Synthesis of non-essential amino acid. Urea synthesis or removal of ammonia. Key Terms acetyl-CoA : a molecule that participates in many biochemical reactions in protein, carbohydrate and lipid metabolism adipose tissue : a term for loose connective tissue composed of adipocytes; its main role is to store energy in the form of fat glycolysis: the metabolic pathway that converts glucose into pyruvate ketone bodies: water-soluble molecules containing the ketone group produced by the liver from fatty acids.
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The present studies were conducted to find whether this action was due to an effect of glucose on the utilization of ketone bodies by adipose tissue. The following results were obtained: 1 Glucose stimulates the uptake of acetoacetate and Dhydroxy-butyrate by adipose tissue, but not by diaphragm muscle.
Insulin enhances this effect of glucose on adipose tissue. Insulin enhances this effect but has no effect in the absence of glucose.
Insulin does not influence the uptake of oxygen in the presence of glucose and acetoacetate. According to these results, adipose tissue is a site for the "peripheral" utilization of ketone bodies.
Published July 1, - More info. The effects of late pregnancy on adipose tissue metabolism have been examined in fed and fasted rats. In the fed state, adipose tissue from pregnant rats displayed an increased content of free fatty acids FFA.
This coincided with augmented cleavage of preformed glycerides during incubation in vitro as evidenced by greater net production of FFA and glycerol, and altered disposition of labeled glucose.
The enhanced lipolysis was independent of the availability of glucose and was not accompanied by impaired responsiveness to the antilipolytic or to the lipogenic actions of added insulin. In the presence of glucose and albumin, esterification as well as lipolysis was greater in adipose tissue from pregnant than nongravid animals.
All the differences were exaggerated by prior fasting. These properties of adipose tissue during late gestation have been ascribed to a primary activation of lipolysis rather than impaired esterification or resistance to insulin.
It has been suggested that the hormones of pregnancy may be responsible. Although increased intake of food and heightened availability of insulin may offset the net lipolytic effects in the fed state, a heightened turnover of adipose stores is always present.
Thus, the pregnant animal appears better poised to mobilize preformed fat whenever exogenous nutrients are withheld. Click on an image below to see the page. View PDF of the complete article.
Interactions between the aadipose of Carbohydrste and lipids provide the basis for a metabolissm of metabolic Nutritional support for injury prevention which have been observed in Leafy green wholesalers and experimental Carblhydrate. Particular examples are abnormalities which may be seen in the storage Micronutrient-rich herbs mobilisation of Tisaue and in the Carbojydrate contribution of glucose and fatty acid to energy needs. The ni caloric restriction and micronutrient balance a Caloric restriction and micronutrient balance Fatty Acid Tiesue is reviewed and forms the basis for recent studies which are outlined. An essential feature of the Cycle is the proposal that the normal relationship between glucose and fatty acid metabolism is reciprocal and not dependent; and that the augmented release of fatty acids for oxidation in muscle and other tissues in diabetes is not primarily due to defective glucose metabolism. The release and oxidation of fatty acids may depend upon lipolysis which may be directly regulated by hormone action and not dependent upon glucose metabolism. It can also depend upon esterification of fatty acids which may involve the metabolism of glucose to glycerol phosphate. Evidence is presented that lipid mobilization in the alloxan-diabetic rat which may be insensitive to inhibition by insulin action is primarily dependent upon activation of lipolysis.
Carbohydrate metabolism in adipose tissue -
These ATPs are supplied from fatty acid catabolism via beta oxidation. Glycogenolysis refers to the breakdown of glycogen.
Glucosephosphate can then progress through glycolysis. Glucagon in the liver stimulates glycogenolysis when the blood glucose is lowered, known as hypoglycemia. Adrenaline stimulates the breakdown of glycogen in the skeletal muscle during exercise.
Glycogenesis refers to the process of synthesizing glycogen. The pentose phosphate pathway is an alternative method of oxidizing glucose. Fructose must undergo certain extra steps in order to enter the glycolysis pathway. Lactose, or milk sugar, consists of one molecule of glucose and one molecule of galactose.
Many steps of carbohydrate metabolism allow the cells to access energy and store it more transiently in ATP. Typically, the complete breakdown of one molecule of glucose by aerobic respiration i. involving glycolysis, the citric-acid cycle and oxidative phosphorylation , the last providing the most energy is usually about 30—32 molecules of ATP.
Hormones released from the pancreas regulate the overall metabolism of glucose. The level of circulatory glucose known informally as "blood sugar" , as well as the detection of nutrients in the Duodenum is the most important factor determining the amount of glucagon or insulin produced.
The release of glucagon is precipitated by low levels of blood glucose, whereas high levels of blood glucose stimulates cells to produce insulin. Because the level of circulatory glucose is largely determined by the intake of dietary carbohydrates, diet controls major aspects of metabolism via insulin.
Regardless of insulin levels, no glucose is released to the blood from internal glycogen stores from muscle cells.
Carbohydrates are typically stored as long polymers of glucose molecules with glycosidic bonds for structural support e. chitin , cellulose or for energy storage e. glycogen , starch. However, the strong affinity of most carbohydrates for water makes storage of large quantities of carbohydrates inefficient due to the large molecular weight of the solvated water-carbohydrate complex.
In most organisms, excess carbohydrates are regularly catabolised to form acetyl-CoA , which is a feed stock for the fatty acid synthesis pathway; fatty acids , triglycerides , and other lipids are commonly used for long-term energy storage.
The hydrophobic character of lipids makes them a much more compact form of energy storage than hydrophilic carbohydrates. Gluconeogenesis permits glucose to be synthesized from various sources, including lipids. In some animals such as termites [20] and some microorganisms such as protists and bacteria , cellulose can be disassembled during digestion and absorbed as glucose.
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Advanced Nutrition and Human Metabolism. Cengage Learning. Archives of Biochemistry and Biophysics. ISSN The effects of late pregnancy on adipose tissue metabolism have been examined in fed and fasted rats.
In the fed state, adipose tissue from pregnant rats displayed an increased content of free fatty acids FFA. This coincided with augmented cleavage of preformed glycerides during incubation in vitro as evidenced by greater net production of FFA and glycerol, and altered disposition of labeled glucose.
The enhanced lipolysis was independent of the availability of glucose and was not accompanied by impaired responsiveness to the antilipolytic or to the lipogenic actions of added insulin. In the presence of glucose and albumin, esterification as well as lipolysis was greater in adipose tissue from pregnant than nongravid animals.
All the differences were exaggerated by prior fasting. These properties of adipose tissue during late gestation have been ascribed to a primary activation of lipolysis rather than impaired esterification or resistance to insulin. It has been suggested that the hormones of pregnancy may be responsible.
Although increased intake of food and heightened availability of insulin may offset the net lipolytic effects in the fed state, a heightened turnover of adipose stores is always present.
Thus, the pregnant animal appears better poised to mobilize preformed fat whenever exogenous nutrients are withheld. Click on an image below to see the page. View PDF of the complete article.
Go to JCI Insight. Overview of central energy metabolic pathways with selected blood serum metabolite patterns according to pubertal stages.
Such a data visualization illustrates a rapid decrease in the level of ketogenesis from the early pubertal stages. These changes were associated with decreased levels of acetate, formate and the major Krebs cycle intermediate citrate, and are indicative of a profound remodeling of fatty acid oxidation in children's metabolism during the transition from early childhood to adolescence.
In contrast to the changes in lipid metabolism, glucose and alanine concentrations increased steadily during puberty, whilst lactate concentration increased primarily in the early period of pubertal development. Such variations in blood biochemical profiles probably reflect changes in energy and carbohydrate metabolism during puberty, with alanine and lactate concentrations reflecting changing activity in the Cori and Cahill cycles.
Throughout puberty, changes in amino acid metabolism are more complex. Overall, children show a decreased blood concentration of several compounds, including glutamate, arginine, and glycine. In addition, complex patterns in the metabolism of branched amino acids BCAA are described.
Whilst circulating levels of BCAA catabolic products decreased during puberty, circulating levels of BCAA evolved differently, and seemed to exhibit sexual dimorphism e. Of note, several other blood amino acid profiles displayed distinct differences between boys and girls in late puberty.
For instance, boys showed a distinct increase in glutamine and proline in late puberty, whilst girls showed decreases in histidine, asparagine, and citrulline Supplementary Figure 4.
Finally, creatinine metabolism shows a consistent pattern throughout puberty, with creatinine concentrations increasing steadily, and more markedly in boys from mid-puberty Supplementary Figure 5. As children grow and develop, changes in metabolism are directly related to total energy requirements e.
Growth and development are associated with complex endocrine changes. This description of puberty-related changes in molecular processes and substrate utilization for energy production significantly extends the existing literature.
Although HbA1c retains a positive association with glucose throughout childhood in our cohort, it is weak, and their trends diverge from 10 years These findings therefore limit the interpretation of HbA1c for the diagnosis of impaired fasting glycemia during childhood and suggest that factors other than glycaemia systematically influence the variance of HbA1c in youth Our additional study reveals stronger associations of fasting glycemia with changes in insulin resistance as well as metabolites when compared to HbA1c, which suggests that analysis of temporal glycemic variations may encapsulate more comprehensively the changes in physiological and metabolite pathways during childhood.
In this uniquely well-characterized cohort of healthy children, the transition from childhood to adolescence was associated with increasing fasting glucose concentrations and a complex remodeling of central energy metabolism, including amino acid and fatty acid molecular pathways.
In the EarlyBird cohort, the gradual rise in the fasting respiratory exchange ratio describes an increased carbohydrate oxidation throughout childhood. Yet, these fasting respiratory exchange ratio values are high in comparison to adults, where fasting respiratory exchange ratio would remain between 0.
Higher fasting respiratory exchange ratio values in adults 29 and in adolescents 30 may be linked to reduced metabolic flexibility i. Whilst there is limited published literature on healthy children, in the Earlybird cohort, we did not see statistically significant differences in fasting respiratory exchange ratio between normoglycemic children and those with impaired fasting glycemia.
Since the maximum values are observed around 11—13 years of age, a period of height growth spurt and important growth in lean mass tissues, our observations may suggest a period of reduced metabolic flexibility during puberty. Finally, a potential limitation in the interpretation of the respiratory exchange ratio is that the measurements were conducted in the fasted state, and conclusions should not necessarily be extrapolated to the post-prandial state.
Prior to puberty, we identified that pre-pubertal children oxidize more fat relative to total energy expenditure than adults and pubertal children, an observation consistent with previous reports In addition, pre-pubertal children are known to oxidize fats preferentially over carbohydrates during low to moderate intensity exercise as well, when compared with post-pubertal children and adults 32 — Boisseau et al.
reported that higher fat oxidation in pre-pubertal children was associated with a distinctive metabolic phenotype, namely increased blood free fatty acid and glycerol, which are indicators of fat mobilization from peripheral stores and increased lipolysis Our study has also shown that pre-pubertal children have higher levels of ketogenesis, as noted by higher serum levels of ketones.
Two ketone bodies, namely 3-D-hydroxybutyrate and acetoacetate, decreased linearly during the first two pubertal stages for both sexes, to reach minima that remained constant throughout the rest of childhood. Ketogenesis is generally stimulated when fatty acid β-oxidation and production of acetyl-CoA exceeds the processing capacity of the Krebs cycle.
The decreased concentration of serum citrate and formate with puberty illustrates the decreased contribution of fatty acids to the pool of acetyl-coA entering the Krebs for energy production.
These patterns describe an overall decreasing fatty acid oxidation, via β-oxidation and ketogenesis, from pre-pubertal to pubertal stage. Whereas 3-D-hydroxybutyrate showed the largest decrease in concentration, levels of acetoacetate remained more stable constant levels , which suggests that there may be different contributions to ketogenesis from protein and lipid metabolism during puberty.
In addition, serum lipoprotein levels in childhood are known to vary with age, as a result of the hormonal changes of puberty, with reports of complex pattern and interactions according to age, gender and insulin resistance 36 — Some studies in normal weight children reported that levels of triglycerides mainly in VLDL increased whereas total cholesterol and LDL-cholesterol decreased during puberty in both sexes 36 , Other reports describe distinct and gender-specific patterns from mid-puberty, namely increased triglycerides and decreased HDL cholesterol in boys, and the opposite pattern in girls Our observations suggest that changes in the serum LDL and VLDL fatty acid signature are positively associated with fasting glycemia throughout childhood.
We previously reported how IR development in the Earlybird cohort was marked by decreased phospholipids mainly in HDL particles and increased LDL fatty acid signature in both males and females in the EarlyBird cohort Such an observation further illustrates the remodeling of lipid mobilization and metabolism that underpins structural growth and changing energy storage 36 , As puberty commences and progresses, there are major changes in many physiological processes, which in turn modify fuel mobilization and utilization 39 , Jones and Kostyak reported higher fat oxidation in children 5—10 years compared with adults—an adaptative process that might support normal growth requirements, such as higher rates of protein synthesis, lipid storage, and bone growth.
Such higher requirements are captured in dietary recommendations for fat consumption, which suggest reduction in fat intake from childhood to adulthood 40 , The novel molecular insights into lipid metabolism before and during puberty, revealed in the present study, may help to further refine the dietary recommendations in terms of quantity and quality of lipids required for optimal growth and development of children before and during puberty.
Girls and boys are indistinguishable in muscle strength until puberty, at which time strength and aerobic performance increases more rapidly in boys 7 , Our analysis also revealed that serum creatinine increased from mid puberty more rapidly in boys than in girls, whilst being negatively correlated with fasting glucose.
It is likely that the gender difference in muscle mass and function is driven primarily by the large difference in free testosterone concentrations that emerges with the onset of puberty However, boys are more insulin sensitive than girls, especially during puberty, and it is possible that differences in the action of insulin may also contribute to gender difference in muscle mass and function.
The gender-specific pattern of creatinine was associated with greater increases in serum leucine, valine, glutamine and proline in boys. Our observations agree with a recent report on whole blood amino acid patterns in puberty from the LIFE Child Cohort by Hirschel et al.
Serum creatinine is known to be affected by age, gender, ethnicity, dietary protein intake, and lean mass Amino acids play a major role as building blocks for protein synthesis and as regulators of key metabolic pathways for cell maintenance and growth Previous studies reported that during puberty, growth is driven by maintaining a greater rate of protein synthesis than that of breakdown 46 , Arslanian et al.
described lower protein oxidation and proteolysis during puberty when compared to pre-puberty, whereas protein synthesis was unchanged In addition, they showed that during puberty whole body proteolysis is resistant to suppression by insulin Blood amino acid concentrations reflect both the availability of amino acids and changes in amino acid influx or efflux between muscle and other tissues as a result of their utilization e.
In particular, proline, alanine, and glutamine are used as a source of energy metabolism through the anaplerotic pathway of the Krebs cycle in skeletal muscle Since the efficiency of carbohydrate oxidation increases during puberty, we may hypothesize that increasing glycolytic metabolism reduces the mobilization of these amino acids into the anaplerotic pathway, and further contributes to higher circulating concentrations.
The observed elevation of blood lactate and alanine concentrations with age reflects changes in the Cori and Cahill cycles. Since Cori and Cahill cycle shuttle lactate and alanine from the muscles to the liver, where the nitrogen enters the urea cycle for gluconeogenesis, this phenotype further illustrates the pubertal changes in glycolytic metabolism.
Last, several metabolites of one-carbon metabolism—glycine, dimethylglycine and creatine—showed a negative association with fasting glucose trajectories. This transmethylation pathway closely interconnects choline, betaine and homocysteine metabolism, and is of major importance for numerous cellular functions, such as DNA methylation, phosphatidylcholine, and protein synthesis 51 , Previous reports described how glycine and dimethylglycine metabolism is linked to glucose homeostasis and diabetes and may be genetically determined In particular, lower circulating levels were associated with lower insulin sensitivity and higher fasting glucose 53 , which is in agreement with our novel observations.
With a potential role of the one-carbon cycle in the developmental origins of T2D 54 , the biological implication of such a signature in the course of childhood would benefit from further clinical investigations.
It is recognized that there are several potential limitations with the present study. Importantly, the sample size was limited, and being an exploratory study, it was not possible to undertake an a priori power calculation. Furthermore, while less-invasive methods for measuring IR, such as the HOMA are well-suited for repeat measurements in cohort studies of children, it is recognized that a potential limitation is that IR measured by HOMA correlates only modestly with clamp-derived measures of IR, and also that HOMA IR already correlates highly with fasting insulin in normoglycaemic subjects 55 , However, if fasting insulin secretion is impaired, the direction of error is that HOMA underestimates IR.
Despite these acknowledged limitations, HOMA is considered as a valid method for measuring IR in pediatric research This study demonstrates that normal pubertal growth and development is accompanied by complex and extensive remodeling of metabolism and fuel oxidation, reflecting the changing energy requirements of puberty.
The full complexity of this process is revealed by blood metabolic profiling. Fasting glycemia increases steadily throughout childhood and is accompanied by increasing concentration of insulin and rising respiratory exchange ratio.
As a result, the fuel economy shifts away from fatty acid oxidation and toward carbohydrate oxidation. The metabolic signatures indicate reduced fatty acid oxidation and ketogenesis, increased flux through Cori and Cahill cycles, and complex changes in amino acids with gender differences reflecting the emerging contrasts in body composition.
There are gradual rises in LDL and VLDL particles and remodeling of one carbon metabolism. All of these changes represent normal physiological development. These findings raise the important question at what point do physiological changes, such as increasing fasting glycemia begin to have pathophysiological consequences and raise concern for future cardiometabolic health?
It is possible to speculate that the metabolic changes we have observed, especially the shift away from fat oxidation, and reduced ketogenesis, is maladaptive in the context of obesity, and may also be liable to perpetuate the obese state.
Therefore, the reduced metabolic flexibility of puberty makes this a vulnerable period for excessive weight gain. Weight gain and obesity further exacerbate the physiological insulin resistance of puberty and fasting glycemia, and will favor atherogenic changes in the lipid profile and pathways, such as one carbon metabolism.
This is in line with our other findings which suggested that weight gain and increasing insulin resistance will exacerbate hyperglycaemia 15 in adolescence, especially in those who also have genetic impairment of pancreatic beta cell function 13 , Finally, these findings will have implications for guidance on child nutrition.
Since fat, protein, and carbohydrate requirements change during pubertal development, this study suggests that macronutrient requirements for optimum healthy growth and development and reduction in risk of cardiometabolic disease may need to take into account metabolic changes at puberty and gender differences.
We speculate that increasing respiratory exchange ratio and reduced ketogenesis may justify reduction in dietary fat relative to carbohydrate at adolescence, in order to reduce the risks of weight gain and insulin resistance.
This nutritional change might be necessary earlier in girls, reflecting their earlier onset of puberty and growth spurt. The avoidance of adolescent weight gain is also emphasized, in view of the maladaptive metabolic effects of insulin resistance, and in order to reduce long term cardiometabolic risks.
Since growth and energy metabolism are dependent also on the presence of small quantities of several micronutrients, further analyses should explore the potential influence of key enzyme cofactors on metabonomic profiles and implications for cardiometabolic risk.
This knowledge has the potential to open-up the development of new and age-specific strategies for the prevention of cardiometabolic disease in children, through more evidence-based guidance on lifestyle and personalized dietary interventions. The datasets presented in this article are not readily available because subject in particular, to ethical and privacy considerations.
Requests to access the datasets should be directed to jonathan. pinkney plymouth. uk and francois-pierre. martin rd. The studies involving human participants were reviewed and approved by Plymouth Local Research Ethics Committee. F-PM designed the study. AJ and F-PM were involved in the acquisition of the data.
OC, F-PM, JH, and JP contributed to the analysis, data interpretation, and drafted the manuscript. JP was guarantor of the work. All authors approved the final version. The authors declare that this study received funding from Bright Future Trust, The Kirby Laing Foundation, Peninsula Medical Foundation, Diabetes UK, the EarlyBird Diabetes Trust, and Nestlé Research.
Nestlé Research had the following involvement with the study: metabonomics data generation and analysis, interpretation of data, writing of this article and decision to submit it for publication.
The other funders were not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication.
JH, JP, and AJ are employees of Plymouth University Peninsula School of Medicine and Dentistry. F-PM and OC are employees of Nestlé Research. JH and AJ have received funding from Nestlé Research. The authors have no other dualities of interest to declare. We acknowledge the life and work of our former colleague Terence Wilkin — , Professor of Endocrinology and Metabolism, whose vision and original thinking led to the creation of the EarlyBird Study and the establishment of the collaboration that made possible the studies reported here.
We thank the EarlyBird children, their parents and all EarlyBird team members for their contribution to the study. We thank Ondine Walter for biobanking, sample handling and preparation at Nestlé, and for support for compliance with the Human Research Act.
We thank Christian Darimont and Jörg Hager for scientific discussion during the preparation of the manuscript. The EarlyBird study was supported by Bright Future Trust, The Kirby Laing Foundation, Peninsula Medical Foundation, Diabetes UK, and the EarlyBird Diabetes Trust.
JH and AJ have received funding from the Nestlé Group. The metabonomic analysis reported in this paper was funded by Nestlé Research. World Health Organization. Global Report on Diabetes. Geneva: World Health Organization Google Scholar.
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Glucose, fructose, and galactose are widely used Carbohyrrate the food industry as sweeteners and food additives. Carbohdrate Sweet potato pie of these carbohydrates has Sweet potato pie identified as Glycogen replenishment for runners possible trigger of non-communicable diseases. These include insulin resistance, obesity, and type 2 diabetes. These sugars induce an energy overload with consequent adipose tissue AT expansion, contributing to the development of obesity and inflammation. Encyclopedia Scholarly Community. Entry Journal Book Video Image About Entry Entry Video Image. Submitted Successfully!
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