A comprehensive review on high -fat diet-induced diabetes mellitus: an epigenetic view

Prasad, Monisha; Rajagopal, Ponnulakshmi; Devarajan, Nalini; Veeraraghavan, Vishnu Priya; Palanisamy, Chella Perumal; Cui, Bo; Patil, Shankargouda; Jayaraman, Selvaraj

doi:10.1016/j.jnutbio.2022.109037

Cited by 34 publications

(25 citation statements)

References 134 publications

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“…Another limitation is that we did not observe whether 36M could inhibit inflammatory factors such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Inflammation and adipocyte-derived factors including TNF-α and IL-6 have been reported to link obesity to T2DM [ 6 , 7 ]. Liu et al reported that CAPE could ameliorate calcification by inhibiting activation of the NLRP3 inflammasome in human aortic valve interstitial cells [ 65 ].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Excess body weight has been recognized as a risk factor for T2DM in which approximately 90% of affected patients are overweight or obese [ 6 , 7 ]. Unhealthy dietary intake, particularly a high-fat (HF) diet, plays a critical role to cause imbalance of glucose and lipid metabolism, which gradually impair the function of major metabolic organs leading to dyslipidemia, hyperinsulinemia, progressive insulin resistance, late pancreatic-cell failure, and T2DM [ 7 , 8 ]. The overwhelming role of HF diet in the formation of metabolic disorders, such as systemic insulin resistance and T2DM, is demonstrated by a variety of experiments performed on humans, rodents, and cell culture models [ 8 , 9 , 10 , 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

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N-Octyl Caffeamide, a Caffeic Acid Amide Derivative, Prevents Progression of Diabetes and Hepatic Steatosis in High-Fat Diet Induced Obese Mice

Liu

Lee

et al. 2022

IJMS

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The underlying pathological mechanisms of diabetes are complicated and varied in diabetic patients, which may lead to the current medications often failing to maintain glycemic control in the long term. Thus, the discovery of diverse new compounds for developing medicines to treat diabetes and its complications are urgently needed. Polyphenols are metabolites of plants and have been employed in the prevention and treatment of a variety of diseases. Caffeic acid phenethyl ester (CAPE) is a category of compounds structurally similar to polyphenols. In this study, we aimed to investigate the antidiabetic activity and potential molecular mechanisms of a novel synthetic CAPE derivative N-octyl caffeamide (36M) using high-fat (HF) diet induced obese mouse models. Our results demonstrate that 36M prevented the progression of diabetes in the HF diet fed obese mice via increasing phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and inhibiting expression of protein tyrosine phosphatase 1B (PTP1B). We also found that 36M could prevent hepatic lipid storage in the HF diet fed mice via inhibition of fatty acid synthase and lipid droplet proteins, including perilipins and Fsp27. In conclusion, 36M is a potential candidate compound that can be developed as AMPK inhibitor and PTP1B inhibitor for treating diabetes and hepatic steatosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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N-Octyl Caffeamide, a Caffeic Acid Amide Derivative, Prevents Progression of Diabetes and Hepatic Steatosis in High-Fat Diet Induced Obese Mice

Liu

Lee

et al. 2022

IJMS

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“…Most of the current studies on the relationship between an HFD and diabetes are cohort studies. An HFD can lead to high type 2 diabetes by affecting glucose and lipid metabolism, which in turn can impair the function of major metabolic organs [ 56 ], including adipose tissue, pancreas, and liver. Table 1 summarizes the relationship between dietary fat and diabetes in human studies.…”

Section: Hfd-induced Diabetes In Animal Models and Humansmentioning

confidence: 99%

The Role of Gut Microbiota in High-Fat-Diet-Induced Diabetes: Lessons from Animal Models and Humans

Wang

2023

Nutrients

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The number of diabetes mellitus patients is increasing rapidly worldwide. Diet and nutrition are strongly believed to play a significant role in the development of diabetes mellitus. However, the specific dietary factors and detailed mechanisms of its development have not been clearly elucidated. Increasing evidence indicates the intestinal microbiota is becoming abundantly apparent in the progression and prevention of insulin resistance in diabetes. Differences in gut microbiota composition, particularly butyrate-producing bacteria, have been observed in preclinical animal models as well as human patients compared to healthy controls. Gut microbiota dysbiosis may disrupt intestinal barrier functions and alter host metabolic pathways, directly or indirectly relating to insulin resistance. In this article, we focus on dietary fat, diabetes, and gut microbiome characterization. The promising probiotic and prebiotic approaches to diabetes, by favorably modifying the composition of the gut microbial community, warrant further investigation through well-designed human clinical studies.

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“…In the Western world, high energy supply, sleep deprivation [ 60 ], sedentary lifestyle, and other environmental stressors [ 61 ] have been blamed for the rapid increase in upper central body obesity (abdominal obesity), particularly among individuals who are genetically predisposed to type 2 diabetes and NAFLD. The increase in NAFLD in neonates in both humans and animals has been largely attributed to their exposure to high levels of NEFA in utero [ 62 , 63 ].…”

Section: Elevated Plasma Nefa Play a Primary Role In Hepatic Insulin ...mentioning

confidence: 99%

Regulation of Insulin Clearance by Non-Esterified Fatty Acids

et al. 2022

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Insulin stores lipid in adipocytes and prevents lipolysis and the release of non-esterified fatty acids (NEFA). Excessive release of NEFA during sustained energy supply and increase in abdominal adiposity trigger systemic insulin resistance, including in the liver, a major site of insulin clearance. This causes a reduction in insulin clearance as a compensatory mechanism to insulin resistance in obesity. On the other hand, reduced insulin clearance in the liver can cause chronic hyperinsulinemia, followed by downregulation of insulin receptor and insulin resistance. Delineating the cause–effect relationship between reduced insulin clearance and insulin resistance has been complicated by the fact that insulin action and clearance are mechanistically linked to insulin binding to its receptors. This review discusses how NEFA mobilization contributes to the reciprocal relationship between insulin resistance and reduced hepatic insulin clearance, and how this may be implicated in the pathogenesis of non-alcoholic fatty liver disease.

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A comprehensive review on high -fat diet-induced diabetes mellitus: an epigenetic view

Cited by 34 publications

References 134 publications

N-Octyl Caffeamide, a Caffeic Acid Amide Derivative, Prevents Progression of Diabetes and Hepatic Steatosis in High-Fat Diet Induced Obese Mice

N-Octyl Caffeamide, a Caffeic Acid Amide Derivative, Prevents Progression of Diabetes and Hepatic Steatosis in High-Fat Diet Induced Obese Mice

The Role of Gut Microbiota in High-Fat-Diet-Induced Diabetes: Lessons from Animal Models and Humans

Regulation of Insulin Clearance by Non-Esterified Fatty Acids

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