Fructose metabolism and metabolic disease

Hannou, Sarah Anissa; Haslam, Danielle E.; McKeown, Nicola M.; Herman, Mark A.

doi:10.1172/jci96702

Cited by 405 publications

(421 citation statements)

References 192 publications

(174 reference statements)

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“…It has been demonstrated that long-term high fructose feeding causes increases in chronic liver inflammation, oxidative stress, and fibrosis. [1] Here, we also uncovered related negative consequences associated with SFO, based on both phenotypic change and biochemical examination. Our collective omics analysis here provides compelling evidence that SFO can induce a surprisingly rapid dyslipidemia.…”

Section: Discussionmentioning

confidence: 93%

“…Nowadays, obesity and dyslipidemia are more common than ever in human history. One of the accepted explanations for their increase and early incidence is over nutrition and lack of physical activity that are key elements of obesity, and the dietary pattern including a fat and fructose rich diet are also thought to be critical . High fructose corn syrup (HFCS), a sweetener made from corn starch, is widely used in food products and beverages.…”

Section: Introductionmentioning

confidence: 99%

“…Although a gradual decrease in the consumption rate has been apparent in the past few years, fructose consumption has gradually increased in Western countries . This increasing rate of caloric intake from high‐fructose containing food and beverages is considered to be a contributory factor to increased dyslipidemia and obesity in developed countries …”

Section: Introductionmentioning

confidence: 99%

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Omics Insights into Metabolic Stress and Resilience of Rats in Response to Short‐term Fructose Overfeeding

Yuan

Zhao

et al. 2019

Molecular Nutrition Food Res

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Scope Considerable evidence supports the view that high‐fructose intake is associated with increased and early incidence of obesity and dyslipidemia. However, knowledge on physiopathological alterations introduced by fructose overconsumption is lacking. Therefore, an integrated omics analysis is carried out to investigate the consequences of short‐term fructose overfeeding (SFO) and identify the underlying molecular mechanisms. Methods and results SFO of rats demonstrates obvious histopathological hepatic lipid accumulation and significant elevation in adiposity, total cholesterol, and fasting plasma glucose levels. Integrated omics analysis demonstrates that SFO disturbed metabolic homeostasis and initiated metabolic stress. Hepatic lipogenesis pathways are also negatively impacted by SFO. Analysis of molecular networks generated by ingenuity pathway analysis (IPA) implicates involvement of the extracellular signal regulated kinase (ERK) signaling pathway in SFO and its consequences. Moreover, it is identified that an inherent negative feedback regulation of hepatic sterol regulatory element binding protein 1 (SREBP1) plays an active role in regulating hepatic de novo lipogenesis. Conclusion The findings indicate that SFO disturbs metabolic homeostasis and that endogenous small molecules positively mediate SFO‐induced metabolic adaption. The results also underline that an inherent regulatory mechanism of resilience occurs in response to fructose overconsumption, suggesting that efforts to maintain resilience can be a promising target to prevent and treat metabolic disorder‐like conditions.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Omics Insights into Metabolic Stress and Resilience of Rats in Response to Short‐term Fructose Overfeeding

Yuan

Zhao

et al. 2019

Molecular Nutrition Food Res

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“…Fructose-6-phosphate can enter the hexosamine pathway [54][55][56] for the generation of glycoproteins and glycolipids, while fructose 1,6-bisphosphate is involved in triglyceride synthesis. 57 Glycolysis is driven by the irreversible reactions of hexokinase (HK), phosphofructokinase (PFK), and pyruvate kinase (PK). 14 Glycolysis also contains numerous points of allosteric regulation.…”

Section: Glycolysismentioning

confidence: 99%

Chemical individuality in T cells: A Garrodian view of immunometabolism

McGuire

2020

Immunological Reviews

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Metabolically quiescent T cells circulate throughout the body in search of antigen.Following engagement of their cognate receptors, T cells undergo metabolic reprogramming to support their activation, differentiation, and ultimately function. In the spirit of Sir Archibald Garrod, this metabolic reprogramming actually imparts a chemical individuality which confers advantage, while in others confers vulnerability, depending upon the milieu. Studying T cell immunometabolism in the context of inborn errors of metabolism allows one to define essential pathways of intermediary metabolism as well metabolic vulnerabilities and plasticity. Inborn errors of metabolism, a class of diseases first named by Garrod, have a long history of being informative for common physiologic and pathologic processes. This endeavor may be accomplished through the study of patients, animal models, and in vitro models of inborn errors of metabolism. In this review, the basics of intermediary metabolism and core metabolic pathways will be discussed, along with their relationship to T cell immunometabolism.Due to their pleiotropic nature, the reader will be specifically directed toward various inborn errors of metabolism which may be helpful for answering important questions about the role of metabolism in T cells. K E Y W O R D Simmunometabolism, inborn errors of metabolism, T cells

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“…1). Fructose uptake in the liver is thought to be mainly operated by the glucose transporter GLUT2, but GLUT5 and GLUT8 may also contribute (Hannou et al 2018). Within the liver, fructose is largely extracted at first pass and rapidly phosphorylated into fructose-1-phosphate by the enzyme fructokinase (also known as ketohexokinase), which is highly specific for fructose.…”

Section: Liver Glycogenmentioning

confidence: 99%

Fructose co‐ingestion to increase carbohydrate availability in athletes

Fuchs

Gonzalez

Loon

2019

The Journal of Physiology

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Carbohydrate availability is important to maximize endurance performance during prolonged bouts of moderate‐ to high‐intensity exercise as well as for acute post‐exercise recovery. The primary form of carbohydrates that are typically ingested during and after exercise are glucose (polymers). However, intestinal glucose absorption can be limited by the capacity of the intestinal glucose transport system (SGLT1). Intestinal fructose uptake is not regulated by the same transport system, as it largely depends on GLUT5 as opposed to SGLT1 transporters. Combining the intake of glucose plus fructose can further increase total exogenous carbohydrate availability and, as such, allow higher exogenous carbohydrate oxidation rates. Ingesting a mixture of both glucose and fructose can improve endurance exercise performance compared to equivalent amounts of glucose (polymers) only. Fructose co‐ingestion can also accelerate post‐exercise (liver) glycogen repletion rates, which may be relevant when rapid (<24 h) recovery is required. Furthermore, fructose co‐ingestion can lower gastrointestinal distress when relatively large amounts of carbohydrate (>1.2 g/kg/h) are ingested during post‐exercise recovery. In conclusion, combined ingestion of fructose with glucose may be preferred over the ingestion of glucose (polymers) only to help trained athletes maximize endurance performance during prolonged moderate‐ to high‐intensity exercise sessions and accelerate post‐exercise (liver) glycogen repletion.

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Fructose metabolism and metabolic disease

Cited by 405 publications

References 192 publications

Omics Insights into Metabolic Stress and Resilience of Rats in Response to Short‐term Fructose Overfeeding

Omics Insights into Metabolic Stress and Resilience of Rats in Response to Short‐term Fructose Overfeeding

Chemical individuality in T cells: A Garrodian view of immunometabolism

Fructose co‐ingestion to increase carbohydrate availability in athletes

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