Diabetogenic Impact of Long-Chain ω-3 Fatty Acids on Pancreatic β-Cell Function and the Regulation of Endogenous Glucose Production

Holness, Mark J.; Greenwood, Gemma K.; Smith, Nicholas D.; Sugden, Mary C.

doi:10.1210/en.2003-0479

Cited by 51 publications

(47 citation statements)

References 56 publications

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“…This different effect could be due to the fact that the very low levels of FO given to rats (2.2% of calories) in the present study inhibited per se PI 3Ј-kinase activity in liver and muscle, whereas a high level of FO (20% of calories) prevented the decrease in PI 3Ј-kinase activity and GLUT4 content in muscle of rats fed a high n-6 PUFA diet (35). Holness et al (13) observed that a low level (7% of calories) of dietary FO substituted into a high-fat diet (20% of calories from saturated fat) induced liver insulin resistance while preventing muscle insulin resistance (13), also demonstrating a tissue-specific effect of LC-n-3 PUFA. It is also possible that dexamethasone had a too-potent effect to be alleviated by a low dose of LC-n-3 PUFA.…”

Section: Discussioncontrasting

confidence: 51%

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Corporeau¹,

Foll²,

Taouis³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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The present work aimed to study in rats whether substitution of a low level of fish oil (FO; 2.2% of calories) into a low-fat diet (6.6% of calories from fat as peanut-rape oil or control diet) 1) has a tissue-specific effect on insulin signaling pathway and 2) prevents dexamethasone-induced alteration of insulin signaling in liver, muscle, and adipose tissue. Sixteen rats were used for study of insulin signaling, and sixteen rats received an oral glucose load (3 g/kg). Eight rats/group consumed control diet or diet containing FO over 5 wk. Four rats from each group received a daily intraperitoneal injection of saline or dexamethasone (1 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) for the last 5 days of feeding. In liver, FO decreased phosphatidylinositol 3Ј-kinase (PI 3Ј-kinase) activity by 54% compared with control diet. A similar result was obtained in muscle. In both liver and muscle, FO clearly amplified the effect of dexamethasone. FO did not alter early steps of insulin signaling, and in muscle GLUT4 protein content remained unaltered. In adipose tissue, FO increased PI 3Ј-kinase activity by 74%, whereas dexamethasone decreased it by 65%; inhibition of PI 3Ј-kinase activity by dexamethasone was similar in rats fed FO or control diet, and GLUT4 protein content was increased by 61% by FO. Glycemic and insulinemic responses to oral glucose were not modified by FO. In conclusion, FO increased PI 3Ј-kinase activity in adipose tissue while inhibiting it in liver and muscle. The maintenance of whole body glucose homeostasis suggests an important role of adipose tissue for control of glucose homeostasis. eicosapentaenoic acid; docosahexaenoic acid; insulin resistance; polyunsaturated fatty acids INSULIN RESISTANCE is a common characteristic of type 2 diabetes, obesity, and metabolic syndrome (31), which results from genetic background and/or environmental factors (39). In patients with type 2 diabetes, liver, skeletal muscle, and adipose tissue are resistant to insulin action (8). In skeletal muscle of patients with type 2 diabetes, tyrosine phosphorylation of insulin receptor (IR) and insulin receptor substrate-1 (IRS-1) and phosphatidylinositol (PI) 3Ј-kinase activity are markedly impaired (5), whereas expressions of IR, IRS-1, or the p85␣ subunit of PI 3Ј-kinase remain unaltered (17). Muscle GLUT4 protein is decreased and GLUT4 translocation is reduced by 90% during hyperinsulinemia (27). These alterations of insulin signaling in muscle participate in the decrease in muscle glucose transport, one of the main features of type 2 diabetes (7). In adipose tissue, basal expression of GLUT4 and IRS-1 are reduced, and upregulation of p85␣ by insulin is completely blunted (11).In rats, a high-fat diet (60% of calories from fat as safflower oil) inhibits liver and muscle PI 3Ј-kinase activity (35). In addition, muscle GLUT4 content and adipose tissue GLUT4 gene expression are reduced (35). These alterations likely explain the impairment of glucose transport in these tissues and at whole body level (33). When fish oil (FO), rich in long-chai...

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Section: Discussioncontrasting

confidence: 51%

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Corporeau¹,

Foll²,

Taouis³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…As diabetes mellitus is considered to be related with a low-grade chronic inflammation, one could assume that fish consumption would be linked with diabetes prevention or control [28]. However, the effects of fish consumption on indices of glycemic control are inconsistent; some have suggested that fish consumption is associated with a decreased risk of type 2 diabetes and obesity and a lower incidence of both coronary heart disease and total mortality, due to its omega-3 fatty acid content, but others have not [29,30]. We observed that fish consumption was positively associated with hyperglycemia, hyperinsulinemia, and insulin resistance in non-diabetic people, and that this association was mainly dependent on BMI status.…”

Section: Discussionmentioning

confidence: 99%

The Relationship between Dietary Habits, Blood Glucose and Insulin Levels among People without Cardiovascular Disease and Type 2 Diabetes; The ATTICA Study

Panagiotakos

Tzima²,

Pitsavos³

et al. 2005

Rev Diabetic Stud

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BACKGROUND: Diet has long been associated with a risk of insulin resistance and poor glycemic control. We sought to investigate the association between food groups and indices of glycemic control in adults without type 2 diabetes and cardiovascular disease. METHODS: During 2001 -2002 we randomly enrolled 1514 men (18-87 years old) and 1528 women (18-89 years old) without evidence of cardiovascular disease from the Attica area of Greece. Of them, 118 men and 92 women were excluded from the present analysis due to a history of diabetes mellitus (type 2). Fasting blood glucose and insulin levels were measured, while dietary habits were evaluated through a semi-quantitative food frequency questionnaire. RESULTS: Red meat consumption was positively associated with hyperglycemia (p = 0.04), hyperinsulinemia (p = 0.04), and HOMA levels (p = 0.03), even after adjusting for BMI and various other potential confounders. The intake of fruits, vegetables, legumes, yogurt and other dairy products was not associated with levels of glycemic control indices. CONCLUSIONS: A higher consumption of red meat and its products may aggravate hyperinsulinemia and insulin resistance in non-diabetic people.

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“…123 There are reports that saturated and trans-fatty acids increase insulin resistance, whereas mono-and poly-unsaturated fats decrease resistance and offer protection against disease. [123][124][125] Therefore, the detrimental effect of a prolonged high fat diet on cognitive performance may, at least in part, be due to abnormalities in glucose regulatory mechanisms.…”

Section: Statins and Admentioning

confidence: 99%

Apolipoprotein E, cholesterol metabolism, diabetes, and the convergence of risk factors for Alzheimer's disease and cardiovascular disease

et al. 2006

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High fat diets and sedentary lifestyles are becoming major concerns for Western countries. They have led to a growing incidence of obesity, dyslipidemia, high blood pressure, and a condition known as the insulin-resistance syndrome or metabolic syndrome. These health conditions are well known to develop along with, or be precursors to atherosclerosis, cardiovascular disease, and diabetes. Recent studies have found that most of these disorders can also be linked to an increased risk of Alzheimer's disease (AD). To complicate matters, possession of one or more apolipoprotein E e4 (APOE e4) alleles further increases the risk or severity of many of these conditions, including AD. ApoE has roles in cholesterol metabolism and Ab clearance, both of which are thought to be significant in AD pathogenesis. The apparent inadequacies of ApoE e4 in these roles may explain the increased risk of AD in subjects carrying one or more APOE e4 alleles. This review describes some of the physiological and biochemical changes that the above conditions cause, and how they are related to the risk of AD. A diversity of topics is covered, including cholesterol metabolism, glucose regulation, diabetes, insulin, ApoE function, amyloid precursor protein metabolism, and in particular their relevance to AD. It can be seen that abnormal lipid, cholesterol and glucose metabolism are consistently indicated as central in the pathophysiology, and possibly the pathogenesis of AD. As diagnosis of mild cognitive impairment and early AD are becoming more reliable, and as evidence is accumulating that health conditions such as diabetes, obesity, and coronary artery disease are risk factors for AD, appropriate changes to diets and lifestyles will likely reduce AD risk, and also improve the prognosis for people already suffering from such conditions.

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Diabetogenic Impact of Long-Chain ω-3 Fatty Acids on Pancreatic β-Cell Function and the Regulation of Endogenous Glucose Production

Cited by 51 publications

References 56 publications

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

The Relationship between Dietary Habits, Blood Glucose and Insulin Levels among People without Cardiovascular Disease and Type 2 Diabetes; The ATTICA Study

Apolipoprotein E, cholesterol metabolism, diabetes, and the convergence of risk factors for Alzheimer's disease and cardiovascular disease

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