Antagonism Between Saturated and Unsaturated Fatty Acids in ROS Mediated Lipotoxicity in Rat Insulin-Producing Cells

Gehrmann, Wiebke; Würdemann, Wiebke; Plötz, Thomas; Jörns, Anne; Lenzen, Sigurd; Elsner, Matthias

doi:10.1159/000430261

Cited by 68 publications

(72 citation statements)

References 58 publications

(69 reference statements)

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“…The dysfunction of pancreatic islet possibly results from downregulation of sterol regulatory element-binding protein (SREBP)-1c-mediated IRS-2/Akt pathway [44]. Palmitate also impairs glucose-stimulated insulin secretion and β-cell function in rat insulin-secreting INS-1 cells [46] and induces H 2 O 2 formation in the peroxisomes of RINm5F insulin-producing cells [47], showing its lipotoxicity in vitro. Furthermore, palmitate exposure may induce apoptosis in isolated islets from humans [43,48], possibly through its receptor cell death-inducing DFF45-like effector b (Cideb) [48].…”

Section: Direct Dangerous Factors Under High Fructose Consumptionmentioning

confidence: 99%

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

2017

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High dietary fructose is a major contributor to insulin resistance and metabolic syndrome, disturbing tissue and organ functions. Fructose is mainly absorbed into systemic circulation by glucose transporter 2 (GLUT2) and GLUT5, and metabolized in liver to produce glucose, lactate, triglyceride (TG), free fatty acid (FFA), uric acid (UA) and methylglyoxal (MG). Its extrahepatic absorption and metabolism also take place. High levels of these metabolites are the direct dangerous factors. During fructose metabolism, ATP depletion occurs and induces oxidative stress and inflammatory response, disturbing functions of local tissues and organs to overproduce inflammatory cytokine, adiponectin, leptin and endotoxin, which act as indirect dangerous factors. Fructose and its metabolites directly and/or indirectly cause oxidative stress, chronic inflammation, endothelial dysfunction, autophagy and increased intestinal permeability, and then further aggravate the metabolic syndrome with tissue and organ dysfunctions. Therefore, this review addresses fructose-induced metabolic syndrome, and the disturbance effects of direct and/or indirect dangerous factors on the functions of liver, adipose, pancreas islet, skeletal muscle, kidney, heart, brain and small intestine. It is important to find the potential correlations between direct and/or indirect risk factors and healthy problems under excess dietary fructose consumption.

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Section: Direct Dangerous Factors Under High Fructose Consumptionmentioning

confidence: 99%

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

2017

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“…It was noted that an increase in intake of plant sources of fats and proteins in the diet would reduce the risk of CAD and DM type 2 (8). Several studies demonstrated that increased intake of mono- and poly-unsaturated fatty acids (MUFAs and PUFAs) and lower intake of saturated and trans-fatty acids are associated with a lower risk of DM type 2 (9-11). …”

Section: Introductionmentioning

confidence: 99%

The Effect of Walnut Oil Consumption on Blood Sugar in Patients With Diabetes Mellitus Type 2

Nezhad

Aghasadeghi

Hakimi

et al. 2016

Int J Endocrinol Metab

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BackgroundPrevalence of diabetes mellitus type 2 (DM) is increasing globally. Considering the potential role of poly-unsaturated fatty acids in prevention of DM type 2 and lipid profiles improvement, some studies have been carried out on walnut. However, there are no studies on control of blood sugar in DM type 2 patients using walnut.ObjectivesThe current study aimed to evaluate the effect of walnut oil on blood sugar in DM type 2 patients.MethodsThis randomized control clinical trial was performed on 100 patients with DM type 2. For the experiment group (n = 50), walnut oil (15 g/day for three months) was added to their diet, while the control group (n = 50) did not undergo any interventions. Before initiation of the experiment and after the experiment, the systolic and diastolic blood pressure (SBP and DBP) levels, fasting blood sugar (FBS) and HbA1c were measured.ResultsThe two groups were not significantly different for SBP, DBP, body weight, and Body Mass Index. HbA1c level decreased significantly in the experiment group by 7.86% ± 21.97 (P = 0.005) from 7.00 ± 1.08 before the intervention to 6.37 ± 1.29 after the intervention. Also, FBS level decreased significantly by 8.24% ± 16.77 (P = 0.001); from 158.37 ± 48.16 before the intervention to 137.91 ± 23.24 after the intervention in the experimental group. These changes in the control group were not significant.ConclusionsConsumption of walnut oil (15 g/day for three months) was shown to improve blood glucose level but, no changes were noted for bodyweight and blood pressure in type two diabetic patients.

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“…However, the mechanism of the proapoptotic action of PA is still poorly understood. Participation of caspases in PA‐induced apoptosis has been reported . Increase in the ROS is the important trigger in this process but also appears to be cell‐type dependent.…”

Section: Discussionmentioning

confidence: 97%

Downregulation of sirtuin 3 by palmitic acid increases the oxidative stress, impairment of mitochondrial function, and apoptosis in liver cells

Sharma

Parihar

et al. 2019

J Biochem & Molecular Tox

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Elevated levels of saturated fatty acids show a strong cytotoxic effect in liver cells. Sirtuin 3 (SIRT3), a mitochondrially localized member of NAD+‐dependent deacetylase has been shown to protect hepatocytes against the oxidative stress. The role of SIRT3 on the cytotoxicity caused by fatty acids in liver cells is not fully understood. The aim of this study was to evaluate the expression level of SIRT3, oxidative stress, and mitochondrial impairments in human hepatoma HepG2 cells exposed to palmitic acid (PA). Our results showed that PA treatment caused the deposition of lipid droplets and resulted in an increased expression of tumor necrosis factor‐α in a dose‐dependent manner. Excessive accumulation of PA induces the reactive oxygen species formation and apoptosis while dissipating the mitochondrial transmembrane potential. The level of SIRT3 expression in both nuclear and mitochondrial fractions in HepG2 cells was decreased with the increase in PA concentrations. However, in the cytosolic fraction, the SIRT3 was undetectable. In conclusion, our results showed that PA caused an increase in inflammation and oxidative stress in HepG2 cells. The exposure of PA also resulted in the decline in transmembrane potential and an increase in apoptosis. The underexpression of nuclear and mitochondrial SIRT3 by PA suggests that the PA target the process that regulates the stress‐related gene expression and mitochondrial functions.

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Antagonism Between Saturated and Unsaturated Fatty Acids in ROS Mediated Lipotoxicity in Rat Insulin-Producing Cells

Cited by 68 publications

References 58 publications

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

The Effect of Walnut Oil Consumption on Blood Sugar in Patients With Diabetes Mellitus Type 2

Downregulation of sirtuin 3 by palmitic acid increases the oxidative stress, impairment of mitochondrial function, and apoptosis in liver cells

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