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Advances in the Relationship Between Diet and Insulin Resistance

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (20 April 2025) | Viewed by 1451

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Guest Editor
Department of Translational Medicine and for Romagna, University of Ferrara, Ferrara, Italy
Interests: relationship between nutrition and metabolic health, dietary fatty acids and lipotoxicity; impact of diet on lipid metabolism and mitochondrial function; molecular mechanisms linking diet
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Special Issue Information

Dear Colleagues,

We would like to invite you to submit your manuscripts to this Special Issue entitled “Advances in the Relationship Between Diet and Insulin Resistance”.

Obesity has become a global health concern considering the epidemic proportions it has reached worldwide and the burden it poses upon health and life span. Indeed, obesity represents a risk factor for a plethora of diseases, including cardiovascular disease, several types of cancer, neurodegenerative disease, and type 2 diabetes mellitus (T2DM). With regard to the latter, obesity fosters insulin resistance which, in turn, is the hallmark of T2DM. Mechanistically, adipocyte overexpansion and dysfunction, due to an increased energy supply, result in lipid spillover from the adipose tissue with the consequent accumulation of fat in tissues not suited for its storage. This phenomenon is called lipotoxicity and represents a key mechanism underpinning the development of insulin resistance. In particular, the intracellular buildup of lipotoxic lipid species such as ceramides and diacylglycerols in metabolically active tissues is able to hamper insulin signal transduction, thereby promoting insulin resistance. In this context, diet quality and energy density are pivotal in promoting body weight gain, adipose tissue dysfunction, and lipotoxicity.

Thus, the aim of this Special Issue is to gather novel insights into the impact of defective lipid metabolism on insulin resistance and whether nutrients, nutraceuticals, and dietary patterns may affect insulin sensitivity by modulating lipid metabolism. As part of this Special Issue, we invite the submission of original manuscripts, as well as meta-analysis, narrative, and systematic reviews, that focus on lipid metabolism in the context of obesity and T2DM. We particularly welcome manuscripts that describe lipidomic studies and provide novel insights into the impact of lipotoxicity on insulin resistance.

Dr. Domenico Sergi
Guest Editor

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Keywords

  • insulin resistance
  • lipotoxicity
  • lipid metabolism
  • type 2 diabetes mellitus
  • dietary lipids
  • lipidomics

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Published Papers (1 paper)

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Research

17 pages, 3016 KiB  
Article
Maternal Low-Protein Diet Leads to Mitochondrial Dysfunction and Impaired Energy Metabolism in the Skeletal Muscle of Male Rats
by Vipin A. Vidyadharan, Ancizar Betancourt, Craig Smith, Chellakkan S. Blesson and Chandra Yallampalli
Int. J. Mol. Sci. 2024, 25(23), 12860; https://doi.org/10.3390/ijms252312860 - 29 Nov 2024
Cited by 2 | Viewed by 1050
Abstract
A prenatal low-protein (LP) diet disrupts glucose homeostasis in adult offspring. Skeletal muscles are one of the main sites of glucose clearance, and mitochondria residing in the muscle fibers are central to glucose homeostasis. Our previous studies indicated that impaired mitochondrial health is [...] Read more.
A prenatal low-protein (LP) diet disrupts glucose homeostasis in adult offspring. Skeletal muscles are one of the main sites of glucose clearance, and mitochondria residing in the muscle fibers are central to glucose homeostasis. Our previous studies indicated that impaired mitochondrial health is central to dysregulated glucose metabolism in the gastrocnemius muscle of the LP-programmed female rats. In addition, dysfunctional mitochondria are often an indicator of underlying irregularities in energy metabolism and metabolic inflexibility. Therefore, this study examined the mitochondrial function and metabolic flexibility in the skeletal muscles of prenatal LP-programmed adult male rats. Pregnant Wistar rats were randomly allotted to a control diet (20% protein) or an isocaloric LP diet (6% protein). Standard laboratory rat chow was given to the dams and the pups after delivery and weaning. Gene and protein expressions, mtDNA copy number, and electron microscopy were assessed in gastrocnemius (GS) muscle, and the mitochondrial oxygen consumption rate was determined using isolated flexor digitorum brevis muscle fibers. The genes associated with mitochondrial outer membrane fusion, mitofusin1 and 2 (Mfn1 and Mfn2), fission (Fis1), and biogenesis (Pgc1B, Nrf1, and Esrra) were lower in the LP group. Further, our functional studies showed that the ATP-linked oxygen consumption rate (OCR), maximal, spare respiratory, and non-mitochondrial respiration-associated OCRs were lower in the LP rats. Further, the mRNA and protein expressions of Ndufb8, a key factor involved in the complex-I catalytic activity, were downregulated in the LP group. In addition, the expression of genes linked to mitochondrial pyruvate transport (Mpc1) and metabolism (Pdha1) was lower in the LP group. In contrast, the expression of mitochondrial fatty acid transporters (Cpt1a and Cpt2) was higher in the LP when compared to the control group. However, electron microscopic analysis exhibited no difference in the mitochondrial ultrastructure in the LP muscle compared to the control. Altogether, our results indicate that the LP diet affects the mitochondrial complex-I integrity and dynamics and leads to altered expression of genes associated with substrate oxidation and mitochondrial dysfunction in the skeletal muscle of the male LP offspring. Full article
(This article belongs to the Special Issue Advances in the Relationship Between Diet and Insulin Resistance)
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