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Impact of Diet Composition on Insulin Resistance—Second Edition

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

Deadline for manuscript submissions: closed (25 June 2024) | Viewed by 1302

Special Issue Editors


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Guest Editor
NOVA Medical School, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, 1169-056 Lisboa, Portugal
Interests: metabolic diseases; neuronal control of metabolism; autonomic nervous system; carotid body; purines
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, 1169-056 Lisboa, Portugal
Interests: metabolic diseases; obesity; insulin resistance; adenosine; liver; brain; adipose tissue; hypercaloric diets; intestinal permeability; gut
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Insulin resistance plays a key role in the pathology of cardiometabolic diseases, which include obesity, hypertension, dyslipidaemia, type 2 diabetes and MAFLD. These diseases are commonly associated with peripheral insulin resistance, which is a problem, as insulin plays a role in the brain circuitries that control food-related behaviour and autonomic activity. Brain insulin resistance is also associated with cognitive impairment, Alzheimer disease and other neurodegenerative diseases.

Disruptions in diet composition (e.g., hypercaloric diets) and patterns, as well as nutritional status, contribute to the genesis of insulin resistance. In contrast, hypocaloric diets, certain feeding regimens and some nutrients have beneficial impacts on insulin resistance and disease development.

This second volume of the Special Issue “Impact of Diet Composition on Insulin Resistance” aims to compile studies that highlight the beneficial or deleterious impacts of different nutritional plans on insulin sensitivity and metabolism, and that unravel the mechanistic links between both diet composition and nutritional status and the development of insulin resistance, both periphery and centrally.

This Special Issue will benefit the scientific and healthcare communities, providing important information about the impacts of food behaviours/nutritional status on whole-body metabolism, and will open new doors to overcoming insulin-resistance-associated diseases by making appropriate and personalised changes to nutritional strategies.

Dr. Silvia V. Conde
Dr. Fatima O. Martins
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

  • insulin
  • food
  • diet
  • nutritional status
  • body metabolism
  • brain

Published Papers (1 paper)

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Research

20 pages, 2753 KiB  
Article
The Effects of Long-Term High Fat and/or High Sugar Feeding on Sources of Postprandial Hepatic Glycogen and Triglyceride Synthesis in Mice
by Ana Reis-Costa, Getachew D. Belew, Ivan Viegas, Ludgero C. Tavares, Maria João Meneses, Bárbara Patrício, Amalia Gastaldelli, Maria Paula Macedo and John G. Jones
Nutrients 2024, 16(14), 2186; https://doi.org/10.3390/nu16142186 - 9 Jul 2024
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Abstract
Background: In MASLD (formerly called NAFLD) mouse models, oversupply of dietary fat and sugar is more lipogenic than either nutrient alone. Fatty acids suppress de novo lipogenesis (DNL) from sugars, while DNL inhibits fatty acid oxidation. How such factors interact to impact hepatic [...] Read more.
Background: In MASLD (formerly called NAFLD) mouse models, oversupply of dietary fat and sugar is more lipogenic than either nutrient alone. Fatty acids suppress de novo lipogenesis (DNL) from sugars, while DNL inhibits fatty acid oxidation. How such factors interact to impact hepatic triglyceride levels are incompletely understood. Methods: Using deuterated water, we measured DNL in mice fed 18-weeks with standard chow (SC), SC supplemented with 55/45-fructose/glucose in the drinking water at 30% (w/v) (HS), high-fat chow (HF), and HF with HS supplementation (HFHS). Liver glycogen levels and its sources were also measured. For HS and HFHS mice, pentose phosphate (PP) fluxes and fructose contributions to DNL and glycogen were measured using [U-13C]fructose. Results: The lipogenic diets caused significantly higher liver triglyceride levels compared to SC. DNL rates were suppressed in HF compared to SC and were partially restored in HFHS but supplied a minority of the additional triglyceride in HFHS compared to HF. Fructose contributed a significantly greater fraction of newly synthesized saturated fatty acids compared to oleic acid in both HS and HFHS. Glycogen levels were not different between diets, but significant differences in Direct and Indirect pathway contributions to glycogen synthesis were found. PP fluxes were similar in HS and HFHS mice and were insufficient to account for DNL reducing equivalents. Conclusions: Despite amplifying the lipogenic effects of fat, the fact that sugar-activated DNL per se barely contributes suggests that its role is likely more relevant in the inhibition of fatty acid oxidation. Fructose promotes lipogenesis of saturated over unsaturated fatty acids and contributes to maintenance of glycogen levels. PP fluxes associated with sugar conversion to fat account for a minor fraction of DNL reducing equivalents. Full article
(This article belongs to the Special Issue Impact of Diet Composition on Insulin Resistance—Second Edition)
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