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Composition of HFP, HFL, HFPS high fat diets.

Composition of HFP, HFL, HFPS high fat diets.

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Relatively little is known about the role of specific saturated fatty acids in the development of high fat diet induced obesity and insulin resistance. Here, we have studied the effect of stearate in high fat diets (45% energy as fat) on whole body energy metabolism and tissue specific insulin sensitivity. C57Bl/6 mice were fed a low stearate diet...

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Context 1
... effect of dietary stearate on whole body energy metabolism To determine whether a high level of dietary stearate induces changes in whole body substrate selection or energy metabolism, three high fat diets were evaluated (table 1): a low stearate diet based on palm oil (HFP, containing 4.4% stearate) and two stearate rich diets based on lard (HFL, containing 15.0% stearate) or the palm oil diet supplemented with tristearin (HFPS, con- taining 13.9% stearate). ...
Context 2
... stearate enrichment of the HFP diet per se induced an adverse metabolic phenotype and hepatic insulin resistance. However, since the FA composition of HFPS and HFL are not identical (table 1), we cannot exclude that other FA's or non fatty acid components of the HFL diet, in addition to stearate, contributed to the induction of hepatic insulin resistance in HFL fed animals. However, although food intake was significantly higher in HFL fed animals compared to HFP fed animals, no differences were found between HFPS and HFP fed animals. ...

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... Respiratory exchange rate (RER) was calculated as VCO 2 /VO 2 . Fat and carbohydrate oxidation rates were calculated according to the following equation [9]: ...
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Background: Differential effects of individual saturated fatty acids (SFAs), particularly stearic acid (C18:0), relative to the shorter-chain SFAs have drawn interest for more accurate nutritional guidelines. However, specific biologic and pathologic functions that can be assigned to particular SFAs are very limited. The present study was designed to compare changes in metabolic and transcriptomic profiles in mice caused by a high C18:0 diet and high palmitic acid (C16:0) diet. Methods: Male C57BL/6 mice were assigned to a normal fat diet (NFD), a high fat diet with high C18:0/C16:0 ratio (HSF) or an isocaloric high fat diet with a low C18:0/C16:0 ratio (LSF) for 10 weeks. An oral glucose tolerance test, 72-h energy expenditure measurement and CT scan of body fat were done before sacrifice. Fasting glucose and lipids were determined by an autobiochemical analyzer. Blood insulin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were measured by enzyme-linked immunosorbent assay methods. Free fatty acids (FFAs) profiles in blood and liver were determined by using gas chromatography-mass spectrometry. Microarray analysis was applied to investigate changes in transcriptomic profiles in the liver. Pathway analysis and gene ontology analysis were applied to describe the roles of differentially expressed mRNAs. Results: Compared with the NFD group, body weight, body fat ratio, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), triglyceride, IL-6, serum and liver FFAs including total FFAs, C16:0 and C18:0 were increased in both high fat diet groups and were much higher in the HSF group than those in the LSF group. Both HSF and LSF mice exhibited distinguishable long non-coding RNA (lncRNA), microRNA and mRNA expression profiles when compared with those of NFD mice. Additionally, more differentially expressed lncRNAs and mRNAs were observed in the HSF group than in the LSF group. Some biological functions and pathways, other than energy metabolism regulation, were identified as differentially expressed mRNAs between the HSF group and the LSF group. Conclusion: The high fat diet with a high C18:0/C16:0 ratio induced more severe glucose and lipid metabolic disorders and inflammation and affected expression of more lncRNAs and mRNAs than an isocaloric low C18:0/C16:0 ratio diet in mice. These results provide new insights into the differences in biological functions and related mechanisms, other than glucose and lipid metabolism, between C16:0 and C18:0.
... For example, palmitic acid (C16:0) and C18:0 are the most common and abundant long chain SFAs in food and human body, and C16:0 can be conversed to C18:0 in the body [8]. A high fat diet with an increase in C18:0 has been found to induce a metabolic state favoring lower oxidative metabolism and severe hepatic insulin resistance in mice, compared with an isocaloric high fat diet [9]. In mice deficient for Elovl6, a gene encoding the elongase that catalyzes the conversion of C16:0 to C18:0, the level of C18:0 decreased while the level of C16:0 increased in serum and liver, and the mice became obese and developed hepatosteatosis, but were protected from insulin resistance when fed a high-fat diet [10]. ...
... Respiratory exchange rate (RER) was calculated as VCO 2 /VO 2 . Fat and carbohydrate oxidation rates were calculated according to the following equation [9]: ...
Preprint
Full-text available
Background: Differential effects of individual saturated fatty acids (SFAs), particularly stearic acid (C18:0) relative to the shorter-chain SFAs have drawn an interest for more accurate nutritional guidelines. But specific biologic and pathologic functions that can be assigned to particular SFAs are very limited. The present study was designed to compare changes in metabolic and transcriptomic profiles in mice caused by high C18:0 diet and high palmitic acid (C16:0) diet. Methods: Male C57BL/6 mice were assigned to a normal fat diet (NFD), a high fat diet with high C18:0 / C16:0 ratio (HSF) or an isocaloric high fat diet with a low C18:0 / C16:0 ratio (LSF) for 10 weeks. Oral glucose tolerance test, 72h-energy expenditure measurement and CT scan of body fat were done before sacrifice. Fasting glucose and lipids were determined by an auto-biochemical analyzer. Blood insulin, tumor necrosis factor-α (TNF-α),and interleukin-6 (IL-6) were measured by enzyme linked immunosorbent assay methods. Free fatty acids (FFAs) profiles in blood and liver were determined by using Gas Chromatography-Mass Spectrometry. Microarray analysis was applied to investigate changes in transcriptomic profiles in liver. Pathway analysis and Gene Ontology analysis were applied to describe the roles of differentially expressed mRNAs. Results: Compared with NFD group, body weight, body fat ratio, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), triglyceride, IL-6, serum and liver FFAs including total FFAs, C16:0 and C18:0 were increased in both high fat diet groups, which were much higher in HSF group than those in LSF group. Both HSF and LSF mice exhibited distinguishable lncRNA, microRNA and mRNA expression profiles, compared with NFD mice. And more differentially expressed lncRNAs and mRNAs were observed in HSF group than those in LSF group. Some biological functions and pathways, other than energy metabolism regulation, were identified that differentially expressed mRNAs between HSF group and LSF group probably involved in. Conclusion: The high fat diet with a high C18:0/C16:0 ratio induced much severe glucose and lipid metabolic disorders and inflammation, and affected more lncRNAs and mRNAs expression than an isocaloric low C18:0/C16:0 ratio diet in mice. These results provide new insights into the different biological functions and related mechanisms, other than glucose and lipid metabolism, between C16:0 and C18:0. Take home message: A high fat diet with a high C18:0/C16:0 ratio probably leads to more changes in multiple biological processes or signaling pathways at transcriptional level than an isocaloric low C18:0/C16:0 ratio diet. The ratio of C18:0/C16:0 in diets should be taken into account for accurate nutrition and health in future.
... For example, palmitic acid (C16:0) and C18:0 are the most common and abundant long chain SFAs in food and the human body, and C16:0 can be converted to C18:0 in the body [8]. A high fat diet with an increase in C18:0 has been found to induce a metabolic state favoring lower oxidative metabolism and severe hepatic insulin resistance in mice compared with an isocaloric high fat diet [9]. In mice deficient for Elovl6, a gene encoding the elongase that catalyzes the conversion of C16:0 to C18:0, the level of C18:0 decreased while the level of C16:0 increased in serum and liver, and the mice became obese and developed hepatosteatosis but were protected from insulin resistance when fed a high fat diet [10]. ...
... Respiratory exchange rate (RER) was calculated as VCO 2 /VO 2 . Fat and carbohydrate oxidation rates were calculated according to the following equation [9]: ...
Preprint
Full-text available
Background: Differential effects of individual saturated fatty acids (SFAs), particularly stearic acid (C18:0), relative to the shorter-chain SFAs have drawn interest for more accurate nutritional guidelines. However, specific biologic and pathologic functions that can be assigned to particular SFAs are very limited. The present study was designed to compare changes in metabolic and transcriptomic profiles in mice caused by a high C18:0 diet and high palmitic acid (C16:0) diet. Methods: Male C57BL/6 mice were assigned to a normal fat diet (NFD), a high fat diet with high C18:0/C16:0 ratio (HSF) or an isocaloric high fat diet with a low C18:0/C16:0 ratio (LSF) for 10 weeks. An oral glucose tolerance test, 72-h energy expenditure measurement and CT scan of body fat were done before sacrifice. Fasting glucose and lipids were determined by an autobiochemical analyzer. Blood insulin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were measured by enzyme-linked immunosorbent assay methods. Free fatty acids (FFAs) profiles in blood and liver were determined by using gas chromatography-mass spectrometry. Microarray analysis was applied to investigate changes in transcriptomic profiles in the liver. Pathway analysis and Gene Ontology analysis were applied to describe the roles of differentially expressed mRNAs. Results: Compared with the NFD group, body weight, body fat ratio, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), triglyceride, IL-6, serum and liver FFAs including total FFAs, C16:0 and C18:0 were increased in both high fat diet groups and were much higher in the HSF group than in the LSF group. Both HSF and LSF mice exhibited distinguishable lncRNA, microRNA and mRNA expression profiles when compared with those of NFD mice. Additionally, more differentially expressed lncRNAs and mRNAs were observed in the HSF group than in the LSF group. Some biological functions and pathways, other than energy metabolism regulation, were identified as differentially expressed mRNAs between the HSF group and LSF group. Conclusion: The high fat diet with a high C18:0/C16:0 ratio induced more severe glucose and lipid metabolic disorders and inflammation and affected expression of more lncRNAs and mRNAs than an isocaloric low C18:0/C16:0 ratio diet in mice. These results provide new insights into the differences in biological functions and related mechanisms, other than glucose and lipid metabolism, between C16:0 and C18:0.
... For example, palmitic acid (C16:0) and C18:0 are the most common and abundant long chain SFAs in food and the human body, and C16:0 can be converted to C18:0 in the body [8]. A high fat diet with an increase in C18:0 has been found to induce a metabolic state favoring lower oxidative metabolism and severe hepatic insulin resistance in mice compared with an isocaloric high fat diet [9]. In mice deficient for Elovl6, a gene encoding the elongase that catalyzes the conversion of C16:0 to C18:0, the level of C18:0 decreased while the level of C16:0 increased in serum and liver, and the mice became obese and developed hepatosteatosis but were protected from insulin resistance when fed a high fat diet [10]. ...
... Respiratory exchange rate (RER) was calculated as VCO 2 /VO 2 . Fat and carbohydrate oxidation rates were calculated according to the following equation [9]: ...
Preprint
Full-text available
Background: Differential effects of individual saturated fatty acids (SFAs), particularly stearic acid (C18:0), relative to the shorter-chain SFAs have drawn interest for more accurate nutritional guidelines. However, specific biologic and pathologic functions that can be assigned to particular SFAs are very limited. The present study was designed to compare changes in metabolic and transcriptomic profiles in mice caused by a high C18:0 diet and high palmitic acid (C16:0) diet. Methods: Male C57BL/6 mice were assigned to a normal fat diet (NFD), a high fat diet with high C18:0/C16:0 ratio (HSF) or an isocaloric high fat diet with a low C18:0/C16:0 ratio (LSF) for 10 weeks. An oral glucose tolerance test, 72-h energy expenditure measurement and CT scan of body fat were done before sacrifice. Fasting glucose and lipids were determined by an autobiochemical analyzer. Blood insulin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were measured by enzyme-linked immunosorbent assay methods. Free fatty acids (FFAs) profiles in blood and liver were determined by using gas chromatography-mass spectrometry. Microarray analysis was applied to investigate changes in transcriptomic profiles in the liver. Pathway analysis and Gene Ontology analysis were applied to describe the roles of differentially expressed mRNAs. Results: Compared with the NFD group, body weight, body fat ratio, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), triglyceride, IL-6, serum and liver FFAs including total FFAs, C16:0 and C18:0 were increased in both high fat diet groups and were much higher in the HSF group than in the LSF group. Both HSF and LSF mice exhibited distinguishable long non-coding RNA (lncRNA), microRNA and mRNA expression profiles when compared with those of NFD mice. Additionally, more differentially expressed lncRNAs and mRNAs were observed in the HSF group than in the LSF group. Some biological functions and pathways, other than energy metabolism regulation, were identified as differentially expressed mRNAs between the HSF group and LSF group. Conclusion: The high fat diet with a high C18:0/C16:0 ratio induced more severe glucose and lipid metabolic disorders and inflammation and affected expression of more lncRNAs and mRNAs than an isocaloric low C18:0/C16:0 ratio diet in mice. These results provide new insights into the differences in biological functions and related mechanisms, other than glucose and lipid metabolism, between C16:0 and C18:0.
... These fatty acids are responsible for insulin resistance, as well as impairing the uptake of glucose by the liver. Furthermore, diets with high levels of stearic acid reduce energy expenditure and consequently increase adiposity (Van den Berg et al., 2010). Therefore, the composition of fatty acids in the diet is more important for checking out metabolic parameters than their overall amount. ...
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... Lipotoxicity is primarily induced by SFAs, such as stearic acid (SA) and palmitic acid (PA) (6,7). For example, although PA induces endoplasmic reticulum stress, inflammation, and insulin resistance (IR) in animal and cell culture models (8), SA likely promotes adiposity and causes IR (9,10). However, the epidemiological results of the relationship between fasting SFA and type 2 diabetes are not consistent (11)(12)(13)(14)(15)(16). ...
... We also found that higher SA induced severe lipotoxicity than any other NEFA (37). In tandem with our report, van de Berg et al. (9) observed reduced hepatic insulin sensitivity as a result Figure 1. OR (95% CI) for development of type 2 diabetes in 6641 men and women who were free of diabetes at baseline according to tertiles (T) of baseline SFA. ...
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Context Experimental evidence suggests saturated fatty acids (SFA) are associated with insulin resistance (IR), but results from epidemiological studies on fasting SFA-diabetes risk are inconsistent. Objective We investigated SFA (fasting and 2h postprandial) profiles and diabetes risk. Design setting A total of 8,940 subjects were recruited for the Harbin People’s Health Study in 2008. Serum SFA (fasting and 2h postprandial) at baseline in Chinese men and women without diabetes were profiled while type 2 diabetes was ascertained using WHO criteria after 4-7 years of follow-up. Outcome Associations between 2h postprandial SFA (2h-SFA) and diabetes. Results At baseline, incident cases of diabetes were older with higher body mass index (BMI) and waist circumference (WC). After a mean follow-up of 6.7 years, 658 incident cases of diabetes occurred. After propensity score (PS) computation and inverse probability of treatment weighting (IPTW) estimation, fasting-SFA were unrelated to diabetes risk but IPTW-adjusted odds ratio (OR) and 95% confidence interval (CI) for the highest tertile of postprandial stearic acid (2h-SA), postprandial palmitic acid (2h-PA) and 2h-SFA for diabetes risk were 2.50 (2.08, 3.16), 1.56 (1.23, 2.02) and 1.70 (1.34, 2.17) respectively P-trend<0.0001. Similarly, 2h-SA/fasting-SA, 2h-PA/fasting-PA and 2h-SFA/fasting-SFA ratios [IPTW-adjusted OR (95%CI): 2.94 (2.39, 3.58), 2.31 (1.80, 2.93), and 2.42 (1.91, 3.11), respectively P-trend<0.0001] predicted the diabetes risk. Conclusions Higher serum 2h-SFA (but not fasting-SFA) independently predicted diabetes risk.
... In rats, diets high in saturated fatty acids (SFAs) have been shown to cause a greater degree of insulin resistance than diets high in monounsaturated fatty acid (MUFA) and polyunsaturated fatty acid (PUFA) (20,158). Different SFA subtypes may also differ in their effects on insulin action with some evidence showing a greater effect of stearate (181). There is also evidence from rodents fed a mixed fatty acid diet that different fatty acid species may have tissue-specific effects on insulin action (190). ...
... The increase we observed in the proportion of VLDL palmitic (16:0) and stearic (18:0) acids, both saturated fatty acids, on the LFD likely reflects an increase in de novo lipogenesis [43]. There is evidence that stearic acid (18:0) in the diet or as free fatty acid induces insulin resistance [44]. Moreover, in a recent cohort study, palmitic (16:0) and stearic (18:0) acids, measured in plasma phospholipids, were positively associated with incident type 2 diabetes [45]. ...
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Purpose We sought to determine the effects of dietary fat on insulin sensitivity and whether changes in insulin sensitivity were explained by changes in abdominal fat distribution or very low-density lipoprotein (VLDL) fatty acid composition. Methods Overweight/obese adults with normal glucose tolerance consumed a control diet (35 % fat/12 % saturated fat/47 % carbohydrate) for 10 days, followed by a 4-week low-fat diet (LFD, n = 10: 20 % fat/8 % saturated fat/62 % carbohydrate) or high-fat diet (HFD, n = 10: 55 % fat/25 % saturated fat/27 % carbohydrate). All foods and their eucaloric energy content were provided. Insulin sensitivity was measured by labeled hyperinsulinemic-euglycemic clamps, abdominal fat distribution by MRI, and fasting VLDL fatty acids by gas chromatography. Results The rate of glucose disposal (Rd) during low- and high-dose insulin decreased on the HFD but remained unchanged on the LFD (Rd-low: LFD: 0.12 ± 0.11 vs. HFD: −0.37 ± 0.15 mmol/min, mean ± SE, p < 0.01; Rd-high: LFD: 0.11 ± 0.37 vs. HFD: −0.71 ± 0.26 mmol/min, p = 0.08). Hepatic insulin sensitivity did not change. Changes in subcutaneous fat were positively associated with changes in insulin sensitivity on the LFD (r = 0.78, p < 0.01) with a trend on the HFD (r = 0.60, p = 0.07), whereas there was no association with intra-abdominal fat. The LFD led to an increase in VLDL palmitic (16:0), stearic (18:0), and palmitoleic (16:1n7c) acids, while no changes were observed on the HFD. Changes in VLDL n-6 docosapentaenoic acid (22:5n6) were strongly associated with changes in insulin sensitivity on both diets (LFD: r = −0.77; p < 0.01; HFD: r = −0.71; p = 0.02). Conclusions A diet very high in fat and saturated fat adversely affects insulin sensitivity and thereby might contribute to the development of type 2 diabetes. ClinicalTrials.gov Identifier NCT00930371.
... Palmitic acid (C16:0) has long been thought to be the major culprit of inflammation, endoplasmic reticulum stress, and insulin resistance (37)(38)(39). Similarly, stearic acid (C18:0) may promote adiposity and induce insulin resistance (40). So far, only a few prospective studies have assessed the associations of the 2 saturated FAs with the incidence of T2DM. ...
Article
Full-text available
Endogenous fatty acid metabolism that results in elongation and desaturation lipid products is thought to play a role in the development of type 2 diabetes mellitus (T2DM). In this study, we evaluated the potential of estimated elongase and desaturase activities for use as predictive markers for T2DM remission after Roux-en-Y gastric bypass (RYGB). The results of a targeted metabolomics approach from 2 independent studies were used to calculate 24 serum FA concentration ratios (product/precursor). Gene expression data from an open public data set was also analyzed. In a longitudinal study of 38 obese diabetic patients with RYGB, we found higher baseline stearic acid/palmitic acid (S/P) ratio. This ratio reflects an elovl6-encoded elongase enzyme activity that has been found to be associated with greater possibility for diabetes remission after RYGB [odds ratio, 2.16 (95% CI 1.10-4.26)], after adjustment for age, gender, body mass index, diabetes duration, glycosylated hemoglobin A1c, and fasting C-peptide. Our results were validated by examination of postsurgical elovl6 gene expression in morbidly obese patients. The association of S/P with the metabolic status of obese individuals was further validated in a cross-sectional cohort of 381 participants. In summary, higher baseline S/P was associated with greater probability of diabetes remission after RYGB and may serve as a diagnostic marker in preoperative patient assessment. - Zhao, L., Ni, Y., Yu, H., Zhang, P., Zhao, A., Bao, Y., Liu, J., Chen, T., Xie G., Panee, J., Chen, W., Rajani, C., Wei, R., Su, M., Jia, Weip., Jia, W. Serum stearic acid/palmitic acid ratio as a potential predictor of diabetes remission after Roux-en-Y gastric bypass in obesity.
... Moreover, the liver-specific effects of V-PYRRO/NO–derived NO release not only attenuated liver steatosis, but were also associated with changes in fatty acid composition, in particular the amelioration of the PUFA/SFA ratio, most likely due to inhibition of endogenous fatty acid synthesis. Our findings are of particular importance because fatty acid saturation has been shown to be involved in the pathogenesis of insulin resistance (van den Berg et al., 2010) and metabolic syndrome (Warensjö et al., 2005). In fact, in our previous work, we demonstrated that the effect of V-PYRRO/NO on insulin resistance and steatosis was mediated by NO-dependent Akt activation and inhibition of de novo fatty acid synthesis by Acetyl-CoA carboxylase (ACC) phosphorylation (Maslak et al., 2015). ...