Influence of dietary fat composition on development of insulin resistance in rats. Relationship to muscle triglyceride and omega-3 fatty acids in muscle phospholipid

Storlien, Leonard H; Jenkins, A. B.; Chisholm, Donald J.; Pascoe, W. S.; Khouri, S.; Kraegen, Edward W.

doi:10.2337/diabetes.40.2.280

Cited by 451 publications

(434 citation statements)

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“…Margarine and oil intake was associated with a reduced diabetes risk in our study, which is in line with the results of previous epidemiological studies that have found an association between the intake of vegetable fat and decreased diabetes risk (Colditz et al, 1992;Vessby et al, 1994;Meyer et al, 2001;Salmeron et al, 2001). The type of dietary fat may play a role in diabetes development by modifying the fatty acid composition of the phospholipid cell membrane, which may affect insulin receptor properties and glucose transportation (Storlien et al, 1991). However, individuals preferring diets high in margarine and oil may be more health conscious, in which case the reduced diabetes risk among them could equally well be due to healthier lifestyles.…”

Section: Discussionsupporting

confidence: 92%

Food consumption and the incidence of type II diabetes mellitus

et al. 2005

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Objective: The consumption of different foods was studied for their ability to predict type II diabetes mellitus. Design: The study design was a cohort study, based on the Finnish Mobile Clinic Health Examination Survey. Setting: A total of 30 communities from different parts of Finland. Subjects: A total of 4304 men and women, 40-69 y of age and free of diabetes at baseline in 1967-1972 and followed up for incidence of diabetes medication during 23 y (383 incident cases). Results: Higher intakes of green vegetables, fruit and berries, oil and margarine, and poultry were found to predict a reduced risk of type II diabetes. The relative risks of developing type II diabetes between the extreme quartiles of the intakes were 0.69 (95% confidence interval (CI) ¼ 0.50-0.93; P for trend (P) ¼ 0.02) for green vegetables, 0.69 (CI ¼ 0.51-0.92; P ¼ 0.03) for fruit and berries, 0.71 (CI ¼ 0.52-0.98; P ¼ 0.01) for margarine and oil, and 0.71 (CI ¼ 0.54-0.94; P ¼ 0.01) for poultry. Conclusion:The results suggest that prevention of type II diabetes might be aided by consumption of certain foods that are rich in nutrients with hypothesized health benefits.

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Section: Discussionsupporting

confidence: 92%

Food consumption and the incidence of type II diabetes mellitus

et al. 2005

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“…To investigate this possibility, we fed lean control mice a 60 % high-fat diet. This type of diet has been shown to cause hepatic insulin resistance in rats after only 3 days of feeding [40,41]. The high-fat diet caused an increase in weight gain compared to mice fed a control diet.…”

Section: Discussionmentioning

confidence: 99%

The biochemical basis of increased hepatic glucose production in a mouse model of type 2 (non-insulin-dependent) diabetes mellitus

Andrikopoulos

Proietto

1995

Diabetologia

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SummaryThe mechanism of increased hepatic glucose production in obese non-insulin-dependent diabetic (NIDDM) patients is unknown. The New Zealand Obese (NZO) mouse, a polygenic model of obesity and NIDDM shows increased hepatic glucose production. To determine the mechanism of this phenomenon, we measured gluconeogenesis from U-s4C -glycerol and U-14C-alanine and relevant gluconeogenic enzymes. Gluconeogenesis from glycerol (0.07 + 0.01 vs 0.21 + 0.02 ~tmol 9 min -~ 9 body mass index (BMI) -1, p < 0.005) and alanine (0.57 + 0.07 vs 0.99 _+ 0.07 ~tmol 9 min -1 9 BMI-I,p < 0.005) was elevated in control mice NZO vs as was glycerol turnover (0.25 + 0.02 vs 0.63 + 0.09 ~tmol 9 min -1 9 BM1-1, p < 0.05). Fructose 1,6-bisphosphatase activity (44.2 + 1.9 vs 55.7 + 4.1 nmol. min-S, mg protein -s, p < 0.05) and protein levels (6.9 + 1.1 vs 16.7 + 2.3 arbitrary units, p < 0.01) were increased in NZO mouse livers, as was the activity of pyruvate carboxylase (0.12 + 0.01 vs 0.17 + 0.02 nmol-min -~ 9 mg protein -s, p < 0.05). To ascertain whether elevated lipid supply is responsible for these biochemical changes in NZO mice, we fed lean control mice a 60 % fat diet for 2 weeks. Fat-fed mice were hyperinsulinaemic (76.37 + 4.06 vs 98.00 + 7.07 pmol/1, p = 0.05) and had elevated plasma non-esterified fatty acid levels (0.44 + 0.05 vs 0.59 _+ 0.03 mmol/1, p = 0.05). Fructose 1,6-bisphosphatase activity (43.86+2.54 vs 52.93 + 3.09 nmol-min -1 -mg protein -1, p = 0.05) and protein levels (33.03 _+ 0.96 vs 40,04 + 1.26 arbitrary units, p = 0.005) and pyruvate carboxylase activity (0.10 + 0.003 vs 0.14 + 0.01 nmol. min -1 -mg protein -1, p < 0.05) were elevated in fat-fed mice. We conclude that in NZO mice increased hepatic glucose production is due to elevated lipolysis resulting from obesity. [Diabetologia (1995[Diabetologia ( ) 38: 1389[Diabetologia ( -1396

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“…Low folate status can result in increased chromosome instability, DNA damage, impaired repair, aberrant DNA methylation and point mutations (Cravo et al, 1994;Fenech et al, 1997;Kim, 1999). These initiate colon carcinogenesis Folic acid (Kim et al, 1996;Newmark et al, 2001;Konings et al, 2002) (2) Insulin resistance/plasma insulin, free fatty acids and triacylglycerol (McKeown-Eyssen, 1994;Giovannucci, 1995;Kim, 1998) Dietary factors including a hypercaloric diet with refined sugars, increased saturated fat, and reduced n-3 fatty acids, together with reduced energy expenditure, increase the accumulation of energy substrates in the body and lead to insulin resistance (Storlien et al, 1991;Tran et al, 1996Tran et al, , 2003Koohestani et al, 1998;Bruce et al, 2000;Kaaks et al, 2000). Insulin resistance is a state of decreased insulin action that is usually accompanied by increased concentrations of: insulin (due to compensatory hypersecretion of insulin), free fatty acid (FFA, due to the impaired antilipolytic action of insulin) and triacylglycerols (TG, derived from the released FFA) (DeFronzo and Ferrannini, 1991).…”

Section: Study Protocolmentioning

confidence: 99%

A pilot randomised controlled trial to reduce colorectal cancer risk markers associated with B-vitamin deficiency, insulin resistance and colonic inflammation

Cirocco

Giacca

et al. 2005

Br J Cancer

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Colorectal cancer risk is associated with biochemical markers for B-vitamin deficiency, insulin resistance and colonic inflammation, suggesting that these three conditions are each involved in colon carcinogenesis. We expected that dietary supplements of folic acid, n-3 fatty acids and calcium would reduce the markers and thus possibly cancer risk. We therefore randomised 98 participants, with previous colonic polyps or intramucosal carcinomas, to a combined treatment of supplementary folic acid, fish oil and calcium carbonate, or placebos for 28 days. Blood and faecal samples were obtained prior to and at the conclusion of the intervention and analysed for plasma folate, homocysteine, insulin, free fatty acids, triglycerides and faecal calprotectin. In addition, plasma vitamin B 12 , thiamin, glucose and C-reactive protein were assessed. Our supplemental strategy modestly affected some of the biomarkers associated with folate metabolism and insulin resistance, but had no effect on those associated with colonic inflammation. This pilot study demonstrates the feasibility and practicality of clinical trials aimed at reducing diet-related biochemical risk markers for colon cancer. We suggest that long-term intervention studies with tumour-related end points should be undertaken when the intervention agents used are found effective in short-term biochemical risk marker trials.

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Influence of dietary fat composition on development of insulin resistance in rats. Relationship to muscle triglyceride and omega-3 fatty acids in muscle phospholipid

Cited by 451 publications

References 0 publications

Food consumption and the incidence of type II diabetes mellitus

Food consumption and the incidence of type II diabetes mellitus

The biochemical basis of increased hepatic glucose production in a mouse model of type 2 (non-insulin-dependent) diabetes mellitus

A pilot randomised controlled trial to reduce colorectal cancer risk markers associated with B-vitamin deficiency, insulin resistance and colonic inflammation

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