Decreased Consumption of Added Fructose Reduces Waist Circumference and Blood Glucose Concentration in Patients with Overweight and Obesity. The DISFRUTE Study: A Randomised Trial in Primary Care

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

The relationship between fructose intake and insulin resistance remains controversial. Our purpose was to determine whether a reduction in dietary fructose is effective in decreasing insulin resistance (HOMA2-IR). This field trial was conducted on 438 adults with overweight and obese status, without diabetes. A total of 121 patients in a low fructose diet (LFD) group and 118 in a standard diet (SD) group completed the 24-week study. Both diets were prescribed with 30–40% of energy intake restriction. There were no between-group differences in HOMA2-IR. However, larger decreases were seen in the LFD group in waist circumference (−7.0 vs. −4.8 = −2.2 cms, 95% CI: −3.7, −0.7) and fasting blood glucose −0.25 vs. −0.11 = −0.14 mmol/L, 95% CI: −0.028, −0.02). The percentage of reduction in calorie intake was similar. Only were differences observed in the % energy intake for some nutrients: total fructose (−2 vs. −0.6 = −1.4, 95% CI: −2.6, −0.3), MUFA (−1.7 vs. −0.4 = −1.3, 95% CI: −2.4, −0.2), protein (5.1 vs. 3.6 = 1.4, 95% CI: 0.1, 2.7). The decrease in fructose consumption originated mainly from the reduction in added fructose (−2.8 vs. −1.9 = −0.9, 95% CI: −1.6, −0.03). These results were corroborated after multivariate adjustments. The low fructose diet did not reduce insulin resistance. However, it reduced waist circumference and fasting blood glucose concentration, which suggests a decrease in hepatic insulin resistance.

Related collections

Most cited references 28

Record: found
Abstract: found
Article: not found

Sugar consumption, metabolic disease and obesity: The state of the controversy.

Kimber L. Stanhope (2016)

The impact of sugar consumption on health continues to be a controversial topic. The objective of this review is to discuss the evidence and lack of evidence that allows the controversy to continue, and why resolution of the controversy is important. There are plausible mechanisms and research evidence that supports the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly. The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, leading to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and high fructose corn syrup (HFCS), which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, CVD and T2DM, often independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0%, 10%, 17.5% or 25% of daily energy requirement (Ereq) as HFCS increased lipid/lipoprotein risk factors for CVD and uric acid in a dose-response manner. However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that enables determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, recent reports conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate. Consumption of excess sugar may also promote the development of CVD and T2DM indirectly by causing increased body weight and fat gain, but this is also a topic of controversy. Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production. Functional magnetic resonance imaging (fMRI) of the brain demonstrates that the brain responds differently to fructose or fructose-containing sugars compared with glucose or aspartame. Some epidemiological studies show that sugar consumption is associated with body weight gain, and there are intervention studies in which consumption of ad libitum high-sugar diets promoted increased body weight gain compared with consumption of ad libitum low- sugar diets. However, there are no studies in which energy intake and weight gain were compared in subjects consuming high or low sugar, blinded, ad libitum diets formulated to ensure both groups consumed a comparable macronutrient distribution and the same amounts of fiber. There is also little data to determine whether the form in which added sugar is consumed, as beverage or as solid food, affects its potential to promote weight gain. It will be very challenging to obtain the funding to conduct the clinical diet studies needed to address these evidence gaps, especially at the levels of added sugar that are commonly consumed. Yet, filling these evidence gaps may be necessary for supporting the policy changes that will help to turn the food environment into one that does not promote the development of obesity and metabolic disease.

0 comments Cited 224 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

Karen Teff, Sharon S Elliott, Matthias Tschöp … (2004)

Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.

0 comments Cited 178 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways.

Martha Cline, Sarita Naik, Brian Roehmholdt … (2013)

Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance. Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety. To study neurophysiological factors that might underlie associations between fructose consumption and weight gain. Twenty healthy adult volunteers underwent 2 magnetic resonance imaging sessions at Yale University in conjunction with fructose or glucose drink ingestion in a blinded, random-order, crossover design. Relative changes in hypothalamic regional cerebral blood flow (CBF) after glucose or fructose ingestion. Secondary outcomes included whole-brain analyses to explore regional CBF changes, functional connectivity analysis to investigate correlations between the hypothalamus and other brain region responses, and hormone responses to fructose and glucose ingestion. There was a significantly greater reduction in hypothalamic CBF after glucose vs fructose ingestion (-5.45 vs 2.84 mL/g per minute, respectively; mean difference, 8.3 mL/g per minute [95% CI of mean difference, 1.87-14.70]; P = .01). Glucose ingestion (compared with baseline) increased functional connectivity between the hypothalamus and the thalamus and striatum. Fructose increased connectivity between the hypothalamus and thalamus but not the striatum. Regional CBF within the hypothalamus, thalamus, insula, anterior cingulate, and striatum (appetite and reward regions) was reduced after glucose ingestion compared with baseline (P < .05 significance threshold, family-wise error [FWE] whole-brain corrected). In contrast, fructose reduced regional CBF in the thalamus, hippocampus, posterior cingulate cortex, fusiform, and visual cortex (P < .05 significance threshold, FWE whole-brain corrected). In whole-brain voxel-level analyses, there were no significant differences between direct comparisons of fructose vs glucose sessions following correction for multiple comparisons. Fructose vs glucose ingestion resulted in lower peak levels of serum glucose (mean difference, 41.0 mg/dL [95% CI, 27.7-54.5]; P < .001), insulin (mean difference, 49.6 μU/mL [95% CI, 38.2-61.1]; P < .001), and glucagon-like polypeptide 1 (mean difference, 2.1 pmol/L [95% CI, 0.9-3.2]; P = .01). In a series of exploratory analyses, consumption of fructose compared with glucose resulted in a distinct pattern of regional CBF and a smaller increase in systemic glucose, insulin, and glucagon-like polypeptide 1 levels.

0 comments Cited 143 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Nutrients

Journal ID (iso-abbrev): Nutrients

Journal ID (publisher-id): nutrients

Title: Nutrients

Publisher: MDPI

ISSN (Electronic): 2072-6643

Publication date (Electronic): 19 April 2020

Publication date Collection: April 2020

Volume: 12

Issue: 4

Electronic Location Identifier: 1149

Affiliations

[1 ]Centro de Salud La Victoria de Acentejo-Tenerife, Calle Domingo Salazar 21, 38380 Tenerife, Canary Islands, Spain

[2 ]Unidad de Investigación de la Gerencia de Atención Primaria de Tenerife y del Hospital Universitario Nuestra Señora de la Candelaria, Santa Cruz de Tenerife, 38310 Tenerife, Canary Islands, Spain

[3 ]Centro de Salud La Victoria de Acentejo, 38380 Tenerife, Canary Islands, Spain; lourdescarrillofernandez@ 123456gmail.com

[4 ]Centro de Salud de Güimar 38500Tenerife, Canary Islands, Spain; jgobierno@ 123456gmail.com

[5 ]Centro de Salud de la Orotava San Antonio, 38313 Tenerife, Canary Islands, Spain; mmendezabad@ 123456gmail.com

[6 ]Centro de Salud Ruiz de Padrón, 38002 Tenerife, Canary Islands, Spain; cborgesalamo@ 123456hotmail.com

[7 ]Laboratorio del Complejo Hospitalario Universitario de Canarias, 38320 La Laguna, Canary Islands, Spain; jgardop@ 123456gobiernodecanarias.org

[8 ]Health Care Research Institute of the Santa Cruz de Tenerife College of Nursing, Colegio Oficial de Enfermeros de Santa Cruz de Tenerife, 38001 Tenerife, Spain; armagujai@ 123456gmail.com

[9 ]European University of the Canary Islands–Member of Laureate International Universities, 38001 Tenerife, Canary Islands, Spain

[10 ]Unidad de Investigación de la Gerencia de Atención Primaria de Tenerife y del Hospital Universitario Nuestra Señora de la Candelaria, Santa Cruz de Tenerife, 38010 Tenerife, Canary Islands, Spain; acableon@ 123456gmail.com

[11 ]Departamento de Medicina Preventiva y Salud Pública de la Universidad de la Laguna, 38200 La Laguna, Canary Island, Spain

Author notes

[* ]Correspondence: sdomcoe@ 123456gobiernodecanarias.org ; Tel.: +34-922-581-900

Author information

Antonio Cabrera-de León https://orcid.org/0000-0003-4745-3405

Article

Publisher ID: nutrients-12-01149

DOI: 10.3390/nu12041149

PMC ID: 7231003

PubMed ID: 32325919

SO-VID: 6dde8a73-b9c5-4a91-8a46-af9655db0661

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Decreased Consumption of Added Fructose Reduces Waist Circumference and Blood Glucose Concentration in Patients with Overweight and Obesity. The DISFRUTE Study: A Randomised Trial in Primary Care

Read this article at

Abstract

Related collections

Karger: Nutrition and Dietetics

Most cited references 28

Sugar consumption, metabolic disease and obesity: The state of the controversy.

Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways.

Author and article information

Journal

Affiliations

Author notes

Author information

Article

History

Categories

Comments

Comment on this article

Similar content 108

Cited by 7

Most referenced authors 1,577