Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes

Around 285 million people worldwide currently have type 2 diabetes and it is projected that this number will be surpassed by 2030. Therefore, it is of the utmost importance to enhance our comprehension of the disease’s development. The regulation of diet, obesity, and inflammation in type 2 diabetes...

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Main Authors: Dequina A. Nicholas, Jacques C. Mbongue, Darysbel Garcia-Pérez, Dane Sorensen, Heather Ferguson Bennit, Marino De Leon, William H. R. Langridge
Format: Article
Language:English
Published: MDPI AG 2024-03-01
Series:Immuno
Subjects:
Online Access:https://www.mdpi.com/2673-5601/4/1/6
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author Dequina A. Nicholas
Jacques C. Mbongue
Darysbel Garcia-Pérez
Dane Sorensen
Heather Ferguson Bennit
Marino De Leon
William H. R. Langridge
author_facet Dequina A. Nicholas
Jacques C. Mbongue
Darysbel Garcia-Pérez
Dane Sorensen
Heather Ferguson Bennit
Marino De Leon
William H. R. Langridge
author_sort Dequina A. Nicholas
collection DOAJ
description Around 285 million people worldwide currently have type 2 diabetes and it is projected that this number will be surpassed by 2030. Therefore, it is of the utmost importance to enhance our comprehension of the disease’s development. The regulation of diet, obesity, and inflammation in type 2 diabetes is believed to play a crucial role in enhancing insulin sensitivity and reducing the risk of onset diabetes. Obesity leads to an increase in visceral adipose tissue, which is a prominent site of inflammation in type 2 diabetes. Dyslipidemia, on the other hand, plays a significant role in attracting activated immune cells such as macrophages, dendritic cells, T cells, NK cells, and B cells to visceral adipose tissue. These immune cells are a primary source of pro-inflammatory cytokines that are believed to promote insulin resistance. This review delves into the influence of elevated dietary free saturated fatty acids and examines the cellular and molecular factors associated with insulin resistance in the initiation of inflammation induced by obesity. Furthermore, it explores novel concepts related to diet-induced inflammation and its relationship with type 2 diabetes.
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spelling doaj.art-38fba84317d249d6bee16decbb9ae1872024-03-27T13:46:47ZengMDPI AGImmuno2673-56012024-03-01419110710.3390/immuno4010006Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 DiabetesDequina A. Nicholas0Jacques C. Mbongue1Darysbel Garcia-Pérez2Dane Sorensen3Heather Ferguson Bennit4Marino De Leon5William H. R. Langridge6School of Biological Sciences, University of California Irvine, Irvine, CA 92697, USADepartment of Biological Sciences, School of Arts and Sciences, Oakwood University, Huntsville, AL 35896, USACenter for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, CA 11085, USACenter for Perinatal Biology, Division of Physiology, Loma Linda School of Medicine, Rm A572, 11234 Anderson Street, Loma Linda, CA 92350, USACenter for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, CA 11085, USACenter for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, CA 11085, USACenter for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, CA 11085, USAAround 285 million people worldwide currently have type 2 diabetes and it is projected that this number will be surpassed by 2030. Therefore, it is of the utmost importance to enhance our comprehension of the disease’s development. The regulation of diet, obesity, and inflammation in type 2 diabetes is believed to play a crucial role in enhancing insulin sensitivity and reducing the risk of onset diabetes. Obesity leads to an increase in visceral adipose tissue, which is a prominent site of inflammation in type 2 diabetes. Dyslipidemia, on the other hand, plays a significant role in attracting activated immune cells such as macrophages, dendritic cells, T cells, NK cells, and B cells to visceral adipose tissue. These immune cells are a primary source of pro-inflammatory cytokines that are believed to promote insulin resistance. This review delves into the influence of elevated dietary free saturated fatty acids and examines the cellular and molecular factors associated with insulin resistance in the initiation of inflammation induced by obesity. Furthermore, it explores novel concepts related to diet-induced inflammation and its relationship with type 2 diabetes.https://www.mdpi.com/2673-5601/4/1/6type 2 diabetesinflammationfatty acidscytokinesadiposeimmune cells
spellingShingle Dequina A. Nicholas
Jacques C. Mbongue
Darysbel Garcia-Pérez
Dane Sorensen
Heather Ferguson Bennit
Marino De Leon
William H. R. Langridge
Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes
Immuno
type 2 diabetes
inflammation
fatty acids
cytokines
adipose
immune cells
title Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes
title_full Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes
title_fullStr Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes
title_full_unstemmed Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes
title_short Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes
title_sort exploring the interplay between fatty acids inflammation and type 2 diabetes
topic type 2 diabetes
inflammation
fatty acids
cytokines
adipose
immune cells
url https://www.mdpi.com/2673-5601/4/1/6
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