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Nutrients
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Fructose Metabolism and Metabolic Health Effects
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Fructose Metabolism and Metabolic Health Effects

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (25 March 2022) | Viewed by 20776

Special Issue Editors

Dr. Samir Softic

E-Mail Website
Guest Editor
Division of Gastroenterology, Hepatology, Nutrition, Department of Pediatrics, University of Kentucky College of Medicine and Kentucky Children's Hospital, Lexington, KY 40506, USA
Interests: obesity; nutrition; insulin resistance; metabolism; lipid metabolism; childhood obesity; carbohydrate metabolism; insulin signaling; metabolic endocrinology; diabetes drug development
Prof. Dr. Miguel A Lanaspa Garcia

E-Mail Website
Guest Editor
Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Boulder, CO 80309, USA
Interests: nephrology
Prof. Dr. Brian J. DeBosch

E-Mail Website
Guest Editor
Departments of Pediatrics and Cell Biology & Physiology, Washington University School of Medicine, St. Louis, MO 63110, USA
Interests: complications; metabolic regulation and obesity; signal transduction/hormone action

Special Issue Information

Dear Colleagues,

There is a worldwide epidemic of obesity, insulin resistance, and metabolic syndrome. Consumption of a high-fat diet was initially proposed to be the driver of the obesity epidemic. As low-fat foods became more popular and in demand, dietary fat was increasingly replaced by another highly palatable food source—refined sugar. However, accumulating evidence suggests that increased sugar consumption may actually be contributing to or driving poor metabolic outcomes associated with obesity.

Renewed interest in sugar metabolism has produced numerous observational studies, linking the intake of dietary sugar with poor metabolic outcomes. In spite of the renewed interest, several questions remain unanswered. First, is dietary sugar simply a vehicle for increased energy intake or is it intrinsically involved in the pathophysiology of obesity? Sugar is generally consumed after meals when subjects are not hungry. Sugar-sweetened beverages are consumed to quench thirst, not hunger. Thus, some suggest that placing a large emphasis on sugar intake is misplaced since increased caloric intake from almost any source will result in obesity. Next, what are the mechanisms linking sugar intake with poor metabolic outcomes? Can we explain on a molecular level why sugar metabolism would negatively affect cellular energy homeostasis? Do different dietary or artificial sugars carry the same metabolic risks? Lastly, can sugar reduction or pharmacologic inhibition of its metabolism serve as a treatment of metabolic dysfunction?

The purpose of this Special Issue is to collect original research reports and review articles that provide the evidence to answer the above questions. Increased understanding of how sugar metabolism affects metabolic outcomes is urgently needed.

Prof. Dr. Samir Softic
Prof. Dr. Miguel A Lanaspa Garcia
Prof. Dr. Brian J. DeBosch
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • sugar
  • fructose
  • obesity
  • insulin resistance
  • metabolism
  • metabolic syndrome
  • NAFLD
  • chronic inflammation
  • nutrient intake
  • kidney disease
  • intestinal nutrient absorption

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 175 KiB  
Editorial
Fructose Metabolism and Metabolic Dysfunction in Adolescents and Young Adults
by Samir Softic, Miguel A. Lanaspa and Brian DeBosch
Nutrients 2023, 15(14), 3162; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15143162 - 16 Jul 2023
Cited by 1 | Viewed by 1415
Abstract
There is a worldwide epidemic of obesity and its associated metabolic dysfunction [...] Full article
(This article belongs to the Special Issue Fructose Metabolism and Metabolic Health Effects)

Research

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22 pages, 2007 KiB  
Article
The Dose-Response Effects of Consuming High Fructose Corn Syrup-Sweetened Beverages on Hepatic Lipid Content and Insulin Sensitivity in Young Adults
by Desiree M. Sigala, Bettina Hieronimus, Valentina Medici, Vivien Lee, Marinelle V. Nunez, Andrew A. Bremer, Chad L. Cox, Candice A. Price, Yanet Benyam, Yasser Abdelhafez, John P. McGahan, Nancy L. Keim, Michael I. Goran, Giovanni Pacini, Andrea Tura, Claude B. Sirlin, Abhijit J. Chaudhari, Peter J. Havel and Kimber L. Stanhope
Nutrients 2022, 14(8), 1648; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14081648 - 15 Apr 2022
Cited by 7 | Viewed by 5337
Abstract
Increased hepatic lipid content and decreased insulin sensitivity have critical roles in the development of cardiometabolic diseases. Therefore, our objective was to investigate the dose-response effects of consuming high fructose corn syrup (HFCS)-sweetened beverages for two weeks on hepatic lipid content and insulin [...] Read more.
Increased hepatic lipid content and decreased insulin sensitivity have critical roles in the development of cardiometabolic diseases. Therefore, our objective was to investigate the dose-response effects of consuming high fructose corn syrup (HFCS)-sweetened beverages for two weeks on hepatic lipid content and insulin sensitivity in young (18–40 years) adults (BMI 18–35 kg/m2). In a parallel, double-blinded study, participants consumed three beverages/day providing 0% (aspartame: n = 23), 10% (n = 18), 17.5% (n = 16), or 25% (n = 28) daily energy requirements from HFCS. Magnetic resonance imaging for hepatic lipid content and oral glucose tolerance tests (OGTT) were conducted during 3.5-day inpatient visits at baseline and again at the end of a 15-day intervention. During the 12 intervening outpatient days participants consumed their usual diets with their assigned beverages. Significant linear dose-response effects were observed for increases of hepatic lipid content (p = 0.015) and glucose and insulin AUCs during OGTT (both p = 0.0004), and for decreases in the Matsuda (p = 0.0087) and Predicted M (p = 0.0027) indices of insulin sensitivity. These dose-response effects strengthen the mechanistic evidence implicating consumption of HFCS-sweetened beverages as a contributor to the metabolic dysregulation that increases risk for nonalcoholic fatty liver disease and type 2 diabetes. Full article
(This article belongs to the Special Issue Fructose Metabolism and Metabolic Health Effects)
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11 pages, 498 KiB  
Article
Dietary Counseling Aimed at Reducing Sugar Intake Yields the Greatest Improvement in Management of Weight and Metabolic Dysfunction in Children with Obesity
by Aurelia Radulescu, Mary Killian, Qiwen Kang, Qingcong Yuan and Samir Softic
Nutrients 2022, 14(7), 1500; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14071500 - 03 Apr 2022
Cited by 4 | Viewed by 2411
Abstract
Pediatric obesity is a significant public health problem, the negative outcomes of which will challenge individual well-being and societal resources for decades to come. The objective of this study was to determine the effects of dietary counseling on weight management and metabolic abnormalities [...] Read more.
Pediatric obesity is a significant public health problem, the negative outcomes of which will challenge individual well-being and societal resources for decades to come. The objective of this study was to determine the effects of dietary counseling on weight management and metabolic abnormalities in children with obesity. One hundred and sixty-five patients aged 2–18 years old were studied over a two and a half year period. Data collected included demographic information, anthropometric assessment, laboratory measurements, and self-reported eating behaviors. Dietary counseling was provided at each visit. The data was analyzed from the first and last visits and the subjects were retrospectively divided into responders and non-responders based on a decrease in their BMI. After receiving dietary guidance, BMI decreased in 44% of the children, and these participants were classified as responders (BMI-R; n = 72). However, BMI did not improve in 56% of the participants, and these were classified as non-responders (BMI-NR; n = 93). At the initial visit, anthropometric measurements and dietary habits were similar between the groups. At the time of the last visit, mean change in BMI was −1.47 (SD 1.31) for BMI-R and +2.40 (SD 9.79) for BMI-NR. Analysis of food intake revealed that BMI-R significantly improved their dietary habits (p = 0.002) by reducing the intake of sugar-sweetened beverages (p = 0.019), processed foods (p = 0.002), sweets (p < 0.001), and unhealthy snacks (p = 0.009), as compared with BMI-NR. There was no change in the intake of second helpings, portion sizes, skipping meals, frequency of meals eaten at school, condiment use, intake of fruits and vegetables and consumption of whole grains between the groups. BMI-R also achieved an improvement in fasted glucose (p = 0.021), triglycerides (p < 0.001), and total cholesterol (p = 0.023), as compared to BMI-NR. In conclusion, children with obesity who were able to decrease their BMI implemented a significant reduction in consumption of foods with high sugar content. Focusing on reducing sugar intake may yield the biggest impact in terms of weight management and the improvement of metabolic abnormalities. Full article
(This article belongs to the Special Issue Fructose Metabolism and Metabolic Health Effects)
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16 pages, 2294 KiB  
Article
A Systems Approach Dissociates Fructose-Induced Liver Triglyceride from Hypertriglyceridemia and Hyperinsulinemia in Male Mice
by Ludivine Doridot, Sarah A. Hannou, Sarah A. Krawczyk, Wenxin Tong, Mi-Sung Kim, Gregory S. McElroy, Alan J. Fowler, Inna I. Astapova and Mark A. Herman
Nutrients 2021, 13(10), 3642; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103642 - 18 Oct 2021
Cited by 3 | Viewed by 3740
Abstract
The metabolic syndrome (MetS), defined as the co-occurrence of disorders including obesity, dyslipidemia, insulin resistance, and hepatic steatosis, has become increasingly prevalent in the world over recent decades. Dietary and other environmental factors interacting with genetic predisposition are likely contributors to this epidemic. [...] Read more.
The metabolic syndrome (MetS), defined as the co-occurrence of disorders including obesity, dyslipidemia, insulin resistance, and hepatic steatosis, has become increasingly prevalent in the world over recent decades. Dietary and other environmental factors interacting with genetic predisposition are likely contributors to this epidemic. Among the involved dietary factors, excessive fructose consumption may be a key contributor. When fructose is consumed in large amounts, it can quickly produce many of the features of MetS both in humans and mice. The mechanisms by which fructose contributes to metabolic disease and its potential interactions with genetic factors in these processes remain uncertain. Here, we generated a small F2 genetic cohort of male mice derived from crossing fructose-sensitive and -resistant mouse strains to investigate the interrelationships between fructose-induced metabolic phenotypes and to identify hepatic transcriptional pathways that associate with these phenotypes. Our analysis indicates that the hepatic transcriptional pathways associated with fructose-induced hypertriglyceridemia and hyperinsulinemia are distinct from those that associate with fructose-mediated changes in body weight and liver triglyceride. These results suggest that multiple independent mechanisms and pathways may contribute to different aspects of fructose-induced metabolic disease. Full article
(This article belongs to the Special Issue Fructose Metabolism and Metabolic Health Effects)
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Review

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14 pages, 5232 KiB  
Review
The Impact of Gut Microbiome on Maternal Fructose Intake-Induced Developmental Programming of Adult Disease
by Chien-Ning Hsu, Hong-Ren Yu, Julie Y. H. Chan, Kay L. H. Wu, Wei-Chia Lee and You-Lin Tain
Nutrients 2022, 14(5), 1031; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14051031 - 28 Feb 2022
Cited by 11 | Viewed by 3081
Abstract
Excessive or insufficient maternal nutrition can influence fetal development and the susceptibility of offspring to adult disease. As eating a fructose-rich diet is becoming more common, the effects of maternal fructose intake on offspring health is of increasing relevance. The gut is required [...] Read more.
Excessive or insufficient maternal nutrition can influence fetal development and the susceptibility of offspring to adult disease. As eating a fructose-rich diet is becoming more common, the effects of maternal fructose intake on offspring health is of increasing relevance. The gut is required to process fructose, and a high-fructose diet can alter the gut microbiome, resulting in gut dysbiosis and metabolic disorders. Current evidence from animal models has revealed that maternal fructose consumption causes various components of metabolic syndrome in adult offspring, while little is known about how gut microbiome is implicated in fructose-induced developmental programming and the consequential risks for developing chronic disease in offspring. This review will first summarize the current evidence supporting the link between fructose and developmental programming of adult diseases. This will be followed by presenting how gut microbiota links to common mechanisms underlying fructose-induced developmental programming. We also provide an overview of the reprogramming effects of gut microbiota-targeted therapy on fructose-induced developmental programming and how this approach may prevent adult-onset disease. Using gut microbiota-targeted therapy to prevent maternal fructose diet-induced developmental programming, we have the potential to mitigate the global burden of fructose-related disorders. Full article
(This article belongs to the Special Issue Fructose Metabolism and Metabolic Health Effects)
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8 pages, 505 KiB  
Review
Maternal Fructose Diet-Induced Developmental Programming
by Michael D. Thompson and Brian J. DeBosch
Nutrients 2021, 13(9), 3278; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13093278 - 20 Sep 2021
Cited by 6 | Viewed by 3619
Abstract
Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing [...] Read more.
Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing relevance. Human studies have identified a clear effect of fructose consumption on maternal health, but little is known of the direct or indirect effects on offspring. Animal models have been utilized to evaluate this concept and an association between maternal fructose and offspring chronic disease, including hypertension and metabolic syndrome. This review will address the mechanisms of developmental programming by maternal fructose and potential options for intervention. Full article
(This article belongs to the Special Issue Fructose Metabolism and Metabolic Health Effects)
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