scholarly journals High Fiber and Beta Carotene from Sweet Potatoes and Pumpkin Improve Insulin Resistance by Inhibition of Sterol Regulatory Binding Protein 1c in Liver of Hypertriglyceridemic Rats

2020 ◽  
Vol 8 (A) ◽  
pp. 898-903
Author(s):  
Sunarti Sunarti ◽  
Umar Santoso ◽  
Abrory Agus Cahya Pramana ◽  
Emy Huriyati ◽  
Dianandha Septiana Rubi
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Binding Protein ◽  
Beta Carotene ◽  
Male Rats ◽  
Standard Diet ◽  
Model Assessment ◽  
High Fat ◽  
High Fiber ◽  
Improve Insulin Resistance

BACKGROUND: High sterol regulatory binding protein 1c (SREBP-1c) gene expression increases triglyceride synthesis, which induces insulin resistance. Short-chain fatty acids (SCFAs) from fiber fermentation and beta carotene may inhibit SREBP-1c gene expression. AIM: The aim of this study was to evaluate the high fiber and beta carotene diet on improving insulin resistance in hypertriglyceridemia rats. METHODS: A total of 25 Wistar male rats were divided into five groups: (1) Normal control (NC); (2) hypertriglyceridemia control (HC); (3) hypertriglyceridemia rats with treatment 1 (HT1); (4) hypertriglyceridemia rats with treatment 2 (HT2); and (5) hypertriglyceridemia rats with treatment 1 (HT3). The HT1, HT2, and HT3 received fiber 1.0 g; 2.0 g; and 3.1 g and beta carotene 725.7 μg; 1451.5 μg; and 2177.2 μg per day, respectively, for 6 weeks. The HC received high fat and fructose diet and the NC received a standard diet. The levels of triglyceride were analyzed using the colorimetric method before and after treatment. At the end of the study, the expression of SREBP-1c was identified by a quantitative polymerase chain reaction. RESULTS: High fat and fructose diet increased the levels of triglyceride (36.53 ± 1.27 vs. 119.79 ± 7.73), but high fiber and beta carotene diet can reduce triglyceride levels in HT1 (94.58 ± 4.53 vs. 77.70 ± 7.97); HT2 (115.58 ± 4.76 vs. 66.90 ± 3.11); and HT3 (103.87 ± 7.47 vs. 62.06 ± 4.45). The decreased triglyceride levels were related to low SREBP-1c gene expression, especially in the liver. Low SREBP-1c gene expression was correlated with homeostatic model assessment of insulin resistance index with r = 0.414; p < 0.05 in the liver and r = 0.158; p > 0.05 in white adipose tissues. CONCLUSION: High fiber and beta carotene diet can improve insulin resistance through inhibition of SREBP-1c gene expression.

scholarly journals Rice Bran Protein Hydrolysates Improve Insulin Resistance and Decrease Pro-inflammatory Cytokine Gene Expression in Rats Fed a High Carbohydrate-High Fat Diet

Nutrients ◽  
2015 ◽  
Vol 7 (8) ◽  
pp. 6313-6329 ◽  
Author(s):  
Kampeebhorn Boonloh ◽  
Veerapol Kukongviriyapan ◽  
Bunkerd Kongyingyoes ◽  
Upa Kukongviriyapan ◽  
Supawan Thawornchinsombut ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Rice Bran ◽  
High Fat Diet ◽  
Inflammatory Cytokine ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
High Fat ◽  
High Carbohydrate ◽  
Improve Insulin Resistance

The effect of aerobic, resistance, and combined training on PPAR-α, SIRT1 gene expression, and insulin resistance in high-fat diet-induced NAFLD male rats

2020 ◽  
Vol 227 ◽  
pp. 113149 ◽  
Author(s):  
Hossein Nikroo ◽  
Seyyed Reza Attarzadeh Hosseini ◽  
Mehrdad Fathi ◽  
Mohammad Ali Sardar ◽  
Majid Khazaei
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
Combined Training ◽  
Sirt1 Gene

scholarly journals Effects of eicosapentaenoic acid ethyl ester on visfatin and apelin in lean and overweight (cafeteria diet-fed) rats

2008 ◽  
Vol 101 (7) ◽  
pp. 1059-1067 ◽  
Author(s):  
Nerea Pérez-Echarri ◽  
Patricia Pérez-Matute ◽  
Beatriz Marcos-Gómez ◽  
J. Alfredo Martínez ◽  
María J. Moreno-Aliaga
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Ethyl Ester ◽  
Negative Relationship ◽  
Cafeteria Diet ◽  
Mrna Levels ◽  
Model Assessment ◽  
High Fat ◽  
G6pase Activity

Previous studies have demonstrated that then-3 fatty acid EPA improves insulin resistance induced by high-fat diets. The aim of the present study was to investigate the potential role of visfatin and apelin in the insulin-sensitising effects of EPA ethyl ester. The effects of EPA on muscle and adipose GLUT mRNA, as well as on liver glucokinase (GK) and glucose-6-phosphatase (G6Pase) activity, were investigated. Male Wistar rats fed on a standard diet or a high-fat cafeteria diet were daily treated by oral administration with EPA ethyl ester (1 g/kg) for 5 weeks. A significant decrease (P < 0·01) in white adipose tissue (WAT) visfatin mRNA levels was found in the cafeteria-fed rats, which was reversed by EPA administration (P < 0·05). Moreover, a negative relationship was observed between homeostatic model assessment (HOMA) and the visfatin:total WAT ratio. In contrast, cafeteria-diet feeding caused a significant increase (P < 0·01) in apelin mRNA in visceral WAT. EPA increased (P < 0·01) apelin gene expression, and a negative relationship between HOMA index with visceral apelin mRNA and serum apelin:total WAT ratio was also observed. EPA treatment did not induce changes in skeletal muscle GLUT1, GLUT4 or insulin receptor mRNA levels. Neither liver GK and G6Pase activity nor the GK:G6Pase ratio was modified by EPA. These data suggest that somehow the insulin-sensitising effects of EPA could be related to its stimulatory action on both visfatin and apelin gene expression in visceral fat, while changes in skeletal muscle GLUT, as well as in hepatic glucose production, are not likely to be the main contributing factors in the improvement in insulin resistance induced by EPA.

scholarly journals Maternal Protein Restriction Altered Insulin Resistance and Inflammation-Associated Gene Expression in Adipose Tissue of Young Adult Mouse Offspring in Response to a High-Fat Diet

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1103 ◽  
Author(s):  
Juhae Kim ◽  
Alee Choi ◽  
Young Hye Kwon
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Serum Insulin ◽  
Protein Restriction ◽  
Epididymal Adipose Tissue ◽  
Model Assessment ◽  
High Fat ◽  
Maternal Protein Restriction ◽  
Increased Risk

Maternal protein restriction is associated with increased risk of insulin resistance and inflammation in adulthood offspring. Here, we investigated whether maternal protein restriction could alter the risk of metabolic syndrome in postweaning high-fat (HF)-diet-challenged offspring, with focus on epididymal adipose tissue gene expression profile. Female ICR mice were fed a control (C) or a low-protein (LP) diet for two weeks before mating and throughout gestation and lactation, and their male offspring were fed an HF diet for 22 weeks (C/HF and LP/HF groups). A subset of offspring of control dams was fed a low-fat control diet (C/C group). In response to postweaning HF diet, serum insulin level and the homeostasis model assessment of insulin resistance (HOMA-IR) were increased in control offspring. Maternal LP diet decreased HOMA-IR and adipose tissue inflammation, and increased serum adiponectin level in the HF-diet-challenged offspring. Accordingly, functional analysis revealed that differentially expressed genes (DEGs) enriched in cytokine production were downregulated in the LP/HF group compared to the C/HF group. We also observed the several annotated gene ontology terms associated with innate immunity and phagocytosis in down-regulated DEGs between LP/HF and C/C groups. In conclusion, maternal protein restriction alleviated insulin resistance and inflammation in young offspring mice fed a HF diet but may impair development of immune system in offspring.

scholarly journals Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet

2010 ◽  
Vol 299 (4) ◽  
pp. R1082-R1090 ◽  
Author(s):  
Jill K. Morris ◽  
Gregory L. Bomhoff ◽  
John A. Stanford ◽  
Paige C. Geiger
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Model ◽  
Locomotor Activity ◽  
Substantia Nigra ◽  
High Fat Diet ◽  
Model Assessment ◽  
High Fat

Despite numerous clinical studies supporting a link between type 2 diabetes (T2D) and Parkinson's disease (PD), the clinical literature remains equivocal. We, therefore, sought to address the relationship between insulin resistance and nigrostriatal dopamine (DA) in a preclinical animal model. High-fat feeding in rodents is an established model of insulin resistance, characterized by increased adiposity, systemic oxidative stress, and hyperglycemia. We subjected rats to a normal chow or high-fat diet for 5 wk before infusing 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Our goal was to determine whether a high-fat diet and the resulting peripheral insulin resistance would exacerbate 6-OHDA-induced nigrostriatal DA depletion. Prior to 6-OHDA infusion, animals on the high-fat diet exhibited greater body weight, increased adiposity, and impaired glucose tolerance. Two weeks after 6-OHDA, locomotor activity was tested, and brain and muscle tissue was harvested. Locomotor activity did not differ between the groups nor did cholesterol levels or measures of muscle atrophy. High-fat-fed animals exhibited higher homeostatic model assessment of insulin resistance (HOMA-IR) values and attenuated insulin-stimulated glucose uptake in fast-twitch muscle, indicating decreased insulin sensitivity. Animals in the high-fat group also exhibited greater DA depletion in the substantia nigra and the striatum, which correlated with HOMA-IR and adiposity. Decreased phosphorylation of HSP27 and degradation of IκBα in the substantia nigra indicate increased tissue oxidative stress. These findings support the hypothesis that a diet high in fat and the resulting insulin resistance may lower the threshold for developing PD, at least following DA-specific toxin exposure.

Abstract 6260: Up-Regulated Expression of MicroRNA-143 in Association with Obesity in the Adipose Tissue of Mice Fed High Fat Diet

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rieko Takanabe ◽  
Koh Ono ◽  
Tomohide Takaya ◽  
Takahiro Horie ◽  
Hiromichi Wada ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Control Cell ◽  
High Fat ◽  
Expression Levels ◽  
Mesenteric Fat ◽  
Regulated Expression

Obesity is the result of an expansion and increase in the number of individual adipocytes. Since changes in gene expression during adipocyte differentiation and hypertrophy are closely associated with insulin resistance and cardiovascular diseases, further insight into the molecular basis of obesity is needed to better understand obesity-associated diseases. MicroRNAs (miRNAs) are approximately 17–24nt single stranded RNA, that post-transcriptionally regulate gene expression. MiRNAs control cell growth, differentiation and metabolism, and may be also involved in pathogenesis and pathophysiology of diseases. It has been proposed that miR-143 plays a role in the differentiation of preadipocytes into mature adipocytes in culture. However, regulated expression of miR-143 in the adult adipose tissue during the development of obesity in vivo is unknown. To solve this problem, C57BL/6 mice were fed with either high-fat diet (HFD) or normal chow (NC). Eight weeks later, severe insulin resistance was observed in mice on HFD. Body weight increased by 35% and the mesenteric fat weight increased by 3.3-fold in HFD mice compared with NC mice. We measured expression levels of miR-143 in the mesenteric fat tissue by real-time PCR and normalized with those of 5S ribosomal RNA. Expression of miR-143 in the mesenteric fat was significantly up-regulated (3.3-fold, p<0.05) in HFD mice compared to NC mice. MiR-143 expression levels were positively correlated with body weight (R=0.577, p=0.0011) and the mesenteric fat weight (R=0.608, p=0.0005). We also measured expression levels in the mesenteric fat of PPARγ and AP2, whose expression are deeply involved in the development of obesity, insulin resistant and arteriosclerosis. The expression levels of miR-143 were closely correlated with those of PPARγ (R=0.600, p=0.0040) and AP2 (R=0.630, p=0.0022). These findings provide the first evidence for up-regulated expression of miR-143 in the mesenteric fat of HFD-induced obese mice, which might contribute to regulated expression of genes involved in the pathophysiology of obesity.

scholarly journals Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α

2007 ◽  
Vol 97 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Nerea Pérez-Echarri ◽  
J. Alfredo Martínez ◽  
Amelia Marti ◽  
María J. Moreno-Aliaga
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Control Diet ◽  
Cafeteria Diet ◽  
High Fat ◽  
Beneficial Effects

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

scholarly journals Evaluation of potential gene expression as early markers of insulin resistance and non-alcoholic fatty liver disease in the Indonesian population

2018 ◽  
Vol 23 (2) ◽  
pp. 84
Author(s):  
Eunice Limantara ◽  
Felicia Kartawidjajaputra ◽  
Antonius Suwanto
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Model Assessment ◽  
Gene Expressions ◽  
Alcoholic Fatty Liver ◽  
Early Markers ◽  
Alcoholic Fatty Liver Disease

Early detection of insulin resistance (IR) or non-alcoholic fatty liver disease (NAFLD) is crucial to preventing future risks of developing chronic diseases. The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), Liver Fat Score (LFS), and Fatty Liver Index (FLI) are generally employed to measure severity stages of IR and NAFLD. The study of gene expressions could explain the molecular mechanisms that occur early on in IR and NAFLD; thus providing potential early markers for both diseases. This study was conducted to evaluate the gene expressions that could potentially be early markers of IR and NAFLD. All participants (n = 21) had normal blood glucose and were categorized as without hepatosteatosis (n = 10), at higher risk of hepatosteatosis (n = 6), and hepatosteatosis (n = 5). Gene expression analysis was performed using the 2-∆∆CT relative quantification method. There were significant differences in galnt2 (p < 0.002) and sirt1 (p < 0.010) expression between the first and the third tertiles of HOMA-IR; and in ptpn1 (p < 0.012) expression between the first and the second tertiles of LFS. In conclusion, the expressions of galnt2 and sirt1 could be used as early markers of IR, while the expression of ptpn1 could be employed as an early marker of NAFLD.

scholarly journals Comparison of high-fat and high-carbohydrate diets for obtaining an experimental model of metabolic syndrome

2021 ◽  
Vol 15 (1) ◽  
pp. 3-14
Author(s):  
T. S. Petryn ◽  
◽  
M. R. Nagalievska ◽  
N. O. Sybirna ◽  
◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Pathological Condition ◽  
Male Rats ◽  
Laboratory Animals ◽  
Atherogenic Dyslipidemia ◽  
Chow Diet ◽  
High Fat ◽  
High Carbohydrate

Introduction. Metabolic syndrome is a cluster of metabolic abnormalities that includes hypertension, central obesity, insulin resistance and atherogenic dyslipidemia. Given the wide geographical distribution and growing number of people suffering from this disease, there is an urgent need in developing animal models that would accurately reproduce the development of all symptoms of human metabolic syndrome (insulin resistance, dyslipidemia, obesity and hypertension). The most cost-effective method related to the real causes of metabolic syndrome is the use of different types of diets. Materials and Methods. The study was performed on white outbred male rats about 6 months old and weighing 300–400 g. The metabolic syndrome was induced by high-fat and high-carbohydrate diets. The lipid-enriched diet involved the consumption of regular chow diet for laboratory animals with additional fat content (40 % by weight of chow). The source of additional lipids was olive oil, which is rich in monounsaturated fatty acids (MUFAs). Animals on the diet enriched in carbohydrates together with regular chow diet for laboratory animals consumed 10 % fructose solution instead of drinking water. Glucose tolerance tests were conducted and areas under the glycemic curves were calculated. We determined the content of glycated hemoglobin and glucose concent­ration, the concentration of low-density lipoproteins (LDL), high-density lipoproteins (HDL), triglycerides and cholesterol in the blood plasma of rats. Results. The development of metabolic syndrome induced by an excessive consumption of carbohydrates and lipids for 42 days was accompanied by impaired glucose tolerance, increased glycosylated hemoglobin, triglycerides and cholesterol concentrations, as well as a decreased HDL content. An increase in the concentrations of LDL and activity of paraoxonase were found due to the induction of the pathological condition by an excessive fat intake, while a high carbohydrate diet caused a decrease in paraoxonase activity. Conclusions. The use of fructose for 42 days causes the most pronounced manifestations of the studied pathology. The use of this model will allow determining the biochemical and molecular changes that accompany the development of this pathological condition. It will also facilitate the development and evaluation of the effectiveness of new therapeutic approaches to the treatment of metabolic syndrome.

scholarly journals Association of vitamin D-binding protein and vitamin D3 with insulin and homeostatic model assessment (HOMA-IR) in overweight and obese females

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Leila Setayesh ◽  
Krista Casazza ◽  
Nariman Moradi ◽  
Sanaz Mehranfar ◽  
Habib Yarizadeh ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitamin D ◽  
Body Composition ◽  
Binding Protein ◽  
The Body ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Assessment ◽  
Vitamin D Binding Protein ◽  
Homeostatic Model Assessment ◽  
Homeostatic Model

Abstract Objective Equivocal association the contribution of 25-hydroxyvitamin D (25(OH)D) and the well-accepted role of vitamin D-binding protein (VDBP) on bioavailability of 25(OH)D or its independent roles, has led to possible association of the VDBP in glucose metabolism. This study was conducted to evaluate the relationships among 25(OH)D, VDBP, glucose/insulin metabolism and homeostatic model assessment (HOMA-IR). Blood samples were collected from 236 obese and overweight women. VDBP and 25(OH)D levels, and biochemical parameters were measured using an enzyme-linked immunosorbent assay (ELISA). An impedance fat analyzer was utilized to acquire the body composition. Results Using the multivariate linear regression, a reverse relationship was observed between VDBP and (HOMA-IR), such that women with higher VDBP displayed lower insulin resistance. The relationship was independent of age, body mass index, standardized energy intake and physical activity (p = 0.00). No significant relationship between 25(OH)D levels, FBS, body composition or insulin resistance were observed (p > 0.2). Current study observed that higher level of VDBP may be associated with lower levels of insulin and HOMA-IR, thus the evaluation of VDBP in diverse population groups seems to have significant clinical value in evaluating the prevalence of DM or early stage of glucose intolerance.

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