Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

Hirata, Takumi; Kawai, Takeshi; Hara, Hiroshi; Tanaka, Kumiko; Kurosawa, Hiroyuki; Fujii, Chieko; Fujita, Haruhisa; Seto, Yoshiko; Matsumoto, Hideo; Itoh, Hiroshi

doi:10.3109/07435800.2015.1038352

Cited by 16 publications

(18 citation statements)

References 31 publications

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“…Previously, we have shown that a palmitic acid-supplemented diet might cause deterioration of glucose tolerance by suppression of insulin secretion from pancreatic β cells in mice [8]. However, there was no difference in the level of palmitic acid among the normal, IGT, and diabetic groups in the current human study (Figure 4).…”

Section: Discussioncontrasting

confidence: 52%

“…Recently, the effects of FFAs on insulin's action have been investigated intensively [5, 6]. We have previously shown that FFAs cause β cell damage mainly by apoptosis in vitro [7] and by ER stress in mice [8]. The serum composition of FFAs in humans differs from race to race, and from environment to environment, because it reflects the average fat intake in the preceding days [9–12].…”

Section: Introductionmentioning

confidence: 99%

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Relationships between Composition of Major Fatty Acids and Fat Distribution and Insulin Resistance in Japanese

Fujii

Kawai

Azuma

et al. 2017

Journal of Diabetes Research

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Objective. The aim of this study was to evaluate the relationships between the composition of free fatty acids (FFAs) and metabolic parameters, including body fat distribution, in Japanese. Methods. The study subjects were 111 Japanese patients (54 males, 57 females). Metabolic parameters and visceral and subcutaneous fat areas as determined by CT scanning at the umbilical level were measured. Glucose tolerance test (GTT) was performed by administering 75 g glucose orally. Results. The percentage of linoleic acid (C18:2), the greatest constituent among FFAs, was negatively correlated with visceral fat area (r = −0.411, p < 0.0001), fasting glucose (r = −0.330, p < 0.0001), HbA1c (r = −0.231, p = 0.0146), and systolic blood pressure (r = −0.224, p = 0.0184). Linoleic acid percentage was also significantly negatively correlated with HOMA-IR (r = −0.416, p < 0.0001) by simple correlation. Based on the findings of OGTT, the 111 subjects were classified into three groups: 33 with normal glucose tolerance, 71 with impaired glucose tolerance (IGT), and 7 diabetic subjects. The percentage of serum linoleic acid in diabetic subjects was significantly lower than that in normal subjects. Conclusion. We conclude that serum linoleic acid level is negatively correlated with the accumulation of visceral fat in relation to a reduction of insulin resistance in Japanese subjects.

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Section: Discussioncontrasting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Relationships between Composition of Major Fatty Acids and Fat Distribution and Insulin Resistance in Japanese

Fujii

Kawai

Azuma

et al. 2017

Journal of Diabetes Research

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“…Dietary supplementation with palmitate for 2 weeks upregulated ER stress markers in mouse Langerhans islets and suppressed glucose-stimulated insulin secretion (GSIS). CHOP, Bip, and XBP1 transcripts were all upregulated [ 70 ]. MIN6 β-cells are exposed to palmitate undergo apoptosis, which is potentiated by XBP1 inhibition [ 71 ].…”

Section: Er Stress Induces Ir and Diabetesmentioning

confidence: 99%

Endoplasmic Reticulum Stress in Metabolic Disorders

Ghemrawi

Battaglia-Hsu

Arnold

2018

Cells

155

113

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Metabolic disorders have become among the most serious threats to human health, leading to severe chronic diseases such as obesity, type 2 diabetes, and non-alcoholic fatty liver disease, as well as cardiovascular diseases. Interestingly, despite the fact that each of these diseases has different physiological and clinical symptoms, they appear to share certain pathological traits such as intracellular stress and inflammation induced by metabolic disturbance stemmed from over nutrition frequently aggravated by a modern, sedentary life style. These modern ways of living inundate cells and organs with saturating levels of sugar and fat, leading to glycotoxicity and lipotoxicity that induce intracellular stress signaling ranging from oxidative to ER stress response to cope with the metabolic insults (Mukherjee, et al., 2015). In this review, we discuss the roles played by cellular stress and its responses in shaping metabolic disorders. We have summarized here current mechanistic insights explaining the pathogenesis of these disorders. These are followed by a discussion of the latest therapies targeting the stress response pathways.

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“…Dietary supplementation with palmitate for 2 weeks upregulated ER stress markers in mouse Langerhans islets and suppressed glucose-stimulated insulin secretion (GSIS). CHOP, BIP and XBP1 transcripts were all up regulated [66]. MIN6 β-cells exposed to palmitate undergo apoptosis, which is potentiated by XBP1 inhibition [67].…”

Section: Lipotoxicitymentioning

confidence: 92%

Endoplasmic Reticulum Stress in Metabolic Disorders

Ghemrawi

Battaglia-Hsu

Arnold

2018

Preprint

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Metabolic disorders have become among the most serious threats to human health, leading to severe chronic diseases such as obesity, type 2 diabetes, non-alcoholic fatty liver disease, as well as cardiovascular diseases. Interestingly, despite the fact that each of these maladies has different physiological and clinical symptoms, they appear to share certain pathological traits such as intracellular stress and inflammation induced by metabolic derangements stemmed from over nutrition frequently aggravated by modern sedentary life style. These modern ways of living inundate cells and organs with saturating levels of sugar and fat, leading to glycotoxicity and lipotoxicity that induce intracellular stress signaling ranging from oxidative to ER stress response to cope with the metabolic insults [1]. In this review, we discuss the roles played by cellular stress and its responses in shaping metabolic disorders. We have summarized here current mechanistic insights explaining the pathogenesis of these disorders. These are followed by a discussion of the latest therapies targeting the stress response pathways.

show abstract

Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

Cited by 16 publications

References 31 publications

Relationships between Composition of Major Fatty Acids and Fat Distribution and Insulin Resistance in Japanese

Relationships between Composition of Major Fatty Acids and Fat Distribution and Insulin Resistance in Japanese

Endoplasmic Reticulum Stress in Metabolic Disorders

Endoplasmic Reticulum Stress in Metabolic Disorders

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