scholarly journals Effects of dietary cis and trans unsaturated and saturated fatty acids on the glucose metabolites and enzymes of rats

2006 ◽  
Vol 95 (5) ◽  
pp. 947-954 ◽  
Author(s):  
Claudio A. Bernal ◽  
Jordi Rovira ◽  
Maryé E. Colandré ◽  
Roser Cussó ◽  
Joan A. Cadefau
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
Saturated Fatty Acid ◽  
High Fat Diet ◽  
Saturated Fatty Acids ◽  
Control Group ◽  
High Fat ◽  
Glucose Metabolites ◽  
Intracellular Glucose

The aim of the present study was to examine whether the level of dietary cis fatty acid (c FA), or the isomers (trans or cis) and/or the saturation of the fatty acids at high dietary fat levels altered the intracellular glucose metabolites and certain regulatory enzyme activities in the skeletal muscle and liver of rats. The animals were fed for 30 d on either a recommended control diet (7% c FA, w/w) or a high-fat diet (20% fatty acids, w/w). The high-fat diet was enriched with either c FA, trans fatty acid (t FA), a moderate proportion of saturated fatty acid (MSFA), or a high proportion of saturated fatty acid (HSFA). The most striking findings were observed in the gastrocnemius muscle with a HSFA diet. There was a significant increase in glucose-6-phosphate (306 %), glucose-1-phosphate (245 %), fructose-6-phosphate (400 %), fructose-1,6-bisphosphate (86 %), glyceraldehyde- 3-phosphate (38 %), pyruvate (341 %), lactate (325 %), citrate (79 %) and the bisphosphorylated sugars as compared with the cFA diet. These changes were paralleled by an increase in muscle triacylglycerol content (49 %) and a decrease in glucose (39 %). In addition, the amount of cFA and the other types of fatty acid (i.e. t FA and MSFA) led to no great differences in glucose metabolism as compared with the respective control group. These data support the hypothesis that glucose changes induced by a HSFA diet are a multifaceted abnormality. Glucose and lactate transport and intracellular glucose metabolism could be the key biochemical defects involved in this detrimental effect on glucose metabolism.

scholarly journals A Trans Fatty Acid Substitute Aggravates Nonalcoholic Steatohepatitis Induced in Mice by Feeding a Choline-Deficient, Methionine-Lowered, L-Amino Acid-Defined, High-Fat Diet

2020 ◽  
Author(s):  
Noriko Suzuki-Kemuriyama ◽  
Akari Abe ◽  
Kinuko Uno ◽  
Shuji Ogawa ◽  
Atsushi Watanabe ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Amino Acid ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Saturated Fatty Acids ◽  
Elevated Serum ◽  
High Fat ◽  
Hepatocellular Apoptosis ◽  
Liver Changes

Abstract Background: Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer. Trans fatty acid (TFA) is hazardous for human health and a risk factor of NASH; thus, efforts have focused on reducing its intake. However, the health benefits of reducing dietary TFA are not fully elucidated. We investigated effects of TFA and its substitute on NASH induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet (CDAA-HF). Methods: Mice were fed CDAA-HF containing shortening with TFA (CDAA-HF-T(+)), CDAA-HF containing shortening with a TFA substitute (CDAA-HF-T(−)), or a control chow for 13/26 weeks. Results: CDAA-HF-T(+) contained TFA, whereas CDAA-HF-T(−) contained no TFA and much saturated fatty acids. CDAA-HF-T(+) and CDAA-HF-T(−) induced NASH in mice, evidenced by elevated serum transaminase activity and liver changes, including steatosis, inflammation, and fibrosis. CDAA-HF-T(−) induced more hepatocellular apoptosis and proliferative (preneoplastic and non-neoplastic) nodular lesions than CDAA-HF-T(+). Conclusions: Thus, replacement of dietary TFA with its substitute does not prevent but aggravates nutritionally induced NASH in mice, at least under the present conditions. Attention should be paid regarding future TFA substitute use in humans, and a fatty acid balance is likely more important than the particular types of fatty acids.

scholarly journals The prolyl hydroxylase PHD3 maintains β-cell glucose metabolism during fatty acid excess

2020 ◽  
Author(s):  
Daniela Nasteska ◽  
Federica Cuozzo ◽  
Alpesh Thakker ◽  
Rula Bany Bakar ◽  
Rebecca Westbrook ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Β Cells ◽  
Β Cell ◽  
Cell Glucose ◽  
Fuel Source

ABSTRACTThe alpha ketoglutarate-dependent dioxygenase, prolyl-4-hydroxylase 3 (PHD3), is a hypoxia-inducible factor target that uses molecular oxygen to hydroxylate proline. While PHD3 has been reported to influence cancer cell metabolism and liver insulin sensitivity, relatively little is known about effects of this highly conserved enzyme in insulin-secreting β-cells. Here, we show that deletion of PHD3 specifically in β-cells (βPHD3KO) is associated with impaired glucose homeostasis in mice fed high fat diet. In the early stages of dietary fat excess, βPHD3KO islets energetically rewire, leading to defects in the management of pyruvate fate and a shift away from glycolysis. However, βPHD3KO islets are able to maintain oxidative phosphorylation and insulin secretion by increasing utilization of fatty acids to supply the tricarboxylic acid cycle. This nutrient-sensing switch cannot be sustained and βPHD3KO islets begin to show signs of failure in response to prolonged metabolic stress, including impaired glucose-stimulated ATP/ADP rises, Ca2+ fluxes and insulin secretion. Thus, PHD3 might be a pivotal component of the β-cell glucose metabolism machinery by suppressing the use of fatty acids as a primary fuel source, under obesogenic and insulin resistant states.SIGNIFICANCE STATEMENTProlyl-4-hydroxylase 3 (PHD3) is involved in the oxygen-dependent regulation of cell phenotype. A number of recent studies have shown that PHD3 might operate at the interface between oxygen availability and metabolism. To understand how PHD3 influences insulin secretion, which depends on intact glucose metabolism, we generated mice lacking PHD3 specifically in pancreatic β-cells. These mice, termed βPHD3KO, are apparently normal until fed high fat diet at which point their β-cells switch to fatty acids as a fuel source. This switch cannot be tolerated and β-cells in βPHD3KO mice eventually fail. Thus, PHD3 maintains glucose-stimulated insulin secretion in β-cells during states of fatty acid excess, such as diabetes and obesity.

scholarly journals Cultured hypothalamic neurons are resistant to inflammation and insulin resistance induced by saturated fatty acids

2010 ◽  
Vol 298 (6) ◽  
pp. E1122-E1130 ◽  
Author(s):  
Sun Ju Choi ◽  
Francis Kim ◽  
Michael W. Schwartz ◽  
Brent E. Wisse
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Saturated Fatty Acid ◽  
Cell Lines ◽  
Saturated Fatty Acids ◽  
Neuronal Cell ◽  
Acid Exposure ◽  
Inflammatory Signaling ◽  
Hypothalamic Neurons

Hypothalamic inflammation induced by high-fat feeding causes insulin and leptin resistance and contributes to the pathogenesis of obesity. Since in vitro exposure to saturated fatty acids causes inflammation and insulin resistance in many cultured cell types, we determined how cultured hypothalamic neurons respond to this stimulus. Two murine hypothalamic neuronal cell cultures, N43/5 and GT1–7, were exposed to escalating concentrations of saturated fatty acids for up to 24 h. Harvested cells were evaluated for activation of inflammation by gene expression and protein content. Insulin-treated cells were evaluated for induction of markers of insulin receptor signaling (p-IRS, p-Akt). In both hypothalamic cell lines, inflammation was induced by prototypical inflammatory mediators LPS and TNFα, as judged by induction of IκBα (3- to 5-fold) and IL-6 (3- to 7-fold) mRNA and p-IκBα protein, and TNFα pretreatment reduced insulin-mediated p-Akt activation by 30% ( P < 0.05). By comparison, neither mixed saturated fatty acid (100, 250, or 500 μM for ≤6 h) nor palmitate exposure alone (200 μM for ≤24 h) caused inflammatory activation or insulin resistance in cultured hypothalamic neurons, whereas they did in control muscle and endothelial cell lines. Despite the lack of evidence of inflammatory signaling, saturated fatty acid exposure in cultured hypothalamic neurons causes endoplasmic reticulum stress, induces mitogen-activated protein kinase, and causes apoptotic cell death with prolonged exposure. We conclude that saturated fatty acid exposure does not induce inflammatory signaling or insulin resistance in cultured hypothalamic neurons. Therefore, hypothalamic neuronal inflammation in the setting of DIO may involve an indirect mechanism mediated by saturated fatty acids on nonneuronal cells.

scholarly journals Effects of dietary fat quantity and composition on fasting and postprandial levels of coagulation factor VII and serum choline-containing phospholipids

2003 ◽  
Vol 90 (2) ◽  
pp. 329-336 ◽  
Author(s):  
Anja Schou Lindman ◽  
Hanne Müller ◽  
Ingebjørg Seljeflot ◽  
Hans Prydz ◽  
Marit Veierød ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Coagulation Factor ◽  
Factor Vii ◽  
High Fat ◽  
Coagulation Factor Vii ◽  
Low Fat Diet

Dietary fat influences plasma levels of coagulation factor VII (FVII) and serum phospholipids (PL). It is, however, unknown if the fat-mediated changes in FVII are linked to PL. The present study aimed to investigate the effects of dietary fat on fasting and postprandial levels of activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII protein (FVIIag) and choline-containing PL (PC). In a randomized single-blinded crossover-designed study a high-fat diet (HSAFA), a low-fat diet (LSAFA), both rich in saturated fatty acids, and a high-fat diet rich in unsaturated fatty acids (HUFA) were consumed for 3 weeks. Twenty-five healthy females, in which postprandial responses were studied in a subset of twelve, were included. The HSAFA diet resulted in higher levels of fasting FVIIa and PC compared with the LSAFA and the HUFA diets (all comparisonsP≤0·01). The fasting PC levels after the LSAFA diet were also higher than after the HUFA diet (P<0·001). Postprandial levels of FVIIa and PC were highest on the HSAFA diet and different from LSAFA and HUFA (all comparisonsP≤0·05). Postprandial FVIIa was higher on the HUFA compared with the LSAFA diet (P<0·03), whereas the HUFA diet resulted in lower postprandial levels of PC than the LSAFA diet (P<0·001). Significant correlations between fasting levels of PC and FVIIc were found on all diets, whereas FVIIag was correlated to PC on the HSAFA and HUFA diet. The present results indicate that dietary fat, both quality and quantity, influences fasting and postprandial levels of FVIIa and PC. Although significant associations between fasting FVII and PC levels were found, our results do not support the assumption that postprandial FVII activation is linked to serum PC.

scholarly journals Saturated Fatty Acid Increases Lung Macrophages and Augments House Dust Mite-Induced Airway Inflammation in Mice Fed with High-Fat Diet

Inflammation ◽  
2017 ◽  
Vol 40 (3) ◽  
pp. 1072-1086 ◽  
Author(s):  
Hiroki Tashiro ◽  
Koichiro Takahashi ◽  
Hironori Sadamatsu ◽  
Go Kato ◽  
Keigo Kurata ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Airway Inflammation ◽  
Saturated Fatty Acid ◽  
House Dust ◽  
House Dust Mite ◽  
High Fat Diet ◽  
High Fat ◽  
Lung Macrophages ◽  
Dust Mite

The effect of high fat diet and saturated fatty acids on insulin signaling in the amygdala and hypothalamus of rats

2013 ◽  
Vol 1537 ◽  
pp. 191-200 ◽  
Author(s):  
Hyoungil Oh ◽  
Stephane Boghossian ◽  
David A. York ◽  
MieJung Park-York
Keyword(s):  
Fatty Acids ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
Saturated Fatty Acids ◽  
High Fat

Plant-Based Diet, Serum Fatty Acid Profile, and Free Radicals in Postmenopausal Women: The Diet and Androgens (DIANA) Randomized Trial

2005 ◽  
Vol 20 (3) ◽  
pp. 169-176 ◽  
Author(s):  
C. Colombo ◽  
P. Muti ◽  
V. Pala ◽  
A. Cavalleri ◽  
E. Venturelli ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Radicals ◽  
Fatty Acid ◽  
Fatty Acid Profile ◽  
Dietary Intervention ◽  
Saturated Fatty Acids ◽  
Intervention Group ◽  
Control Group ◽  
Reactive Oxygen Metabolites ◽  
Serum Fatty Acid

High calorie and fat consumption and the production of free radicals are two major mechanistic pathways between diet and disease. In this study we evaluated the effect of a plant-based diet poor in animal fat and rich in (n-3) fatty acids on fatty acids of serum phospholipids and on the production of reactive oxygen metabolites (ROMs). One hundred and four healthy female postmenopausal volunteers were recruited and randomized to a dietary intervention or a control group. Dietary intervention included a program of food education and biweekly common meals for 18 weeks. When the intervention and control groups were compared, it was seen that dietary intervention resulted in a significant reduction of saturated fatty acids (-1.5%) and a significant increase in (n-3) fatty acids (+20.6%), in particular docosahexaenoic acid (+24.8%). We observed that arachidonic acid decreased (–7.7%), while (n-6) fatty acids did not, and the (n-3)/(n-6) polyunsaturated ratio increased significantly (+24.1%). As expected, ROMs decreased significantly in the intervention group (-6%). The results indicated that a plant-based diet can improve the serum fatty acid profile and decrease ROMs production. These results suggest that a plant-based diet may reduce the body's exposure to oxidative stress.

scholarly journals Dietary Polyunsaturated Fatty Acids Increase Survival and Decrease Bacterial Load during Septic Staphylococcus aureus Infection and Improve Neutrophil Function in Mice

2014 ◽  
Vol 83 (2) ◽  
pp. 514-521 ◽  
Author(s):  
Sara L. Svahn ◽  
Louise Grahnemo ◽  
Vilborg Pálsdóttir ◽  
Intawat Nookaew ◽  
Karl Wendt ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Bacterial Infections ◽  
Saturated Fatty Acids ◽  
Bacterial Load ◽  
Neutrophil Function ◽  
High Fat ◽  
Content Type

Severe infection, including sepsis, is an increasing clinical problem that causes prolonged morbidity and substantial mortality. At present, antibiotics are essentially the only pharmacological treatment for sepsis. The incidence of resistance to antibiotics is increasing; therefore, it is critical to find new therapies for sepsis.Staphylococcus aureusis a major cause of septic mortality. Neutrophils play an important role in the defense against bacterial infections. We have shown that a diet with high levels of dietary saturated fatty acids decreases survival in septic mice, but the mechanisms behind this remain elusive. The aim of the present study was to investigate how the differences in dietary fat composition affect survival and bacterial load after experimental septic infection and neutrophil function in uninfected mice. We found that, afterS. aureusinfection, mice fed a polyunsaturated high-fat diet (HFD-P) for 8 weeks had increased survival and decreased bacterial load during sepsis compared with mice fed a saturated high-fat diet (HFD-S), similar to mice fed a low-fat diet (LFD). Uninfected mice fed HFD-P had a higher frequency of neutrophils in bone marrow than mice fed HFD-S. In addition, mice fed HFD-P had a higher frequency of neutrophils recruited to the site of inflammation in response to peritoneal injection of thioglycolate than mice fed HFD-S. Differences between the proportion of dietary protein and carbohydrate did not affect septic survival at all. In conclusion, polyunsaturated dietary fat increased both survival and efficiency of bacterial clearance during septicS. aureusinfection. Moreover, this diet increased the frequency and chemotaxis of neutrophils, key components of the immune response toS. aureusinfections.

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