scholarly journals Pathophysiology of high fat diet induced obesity: impact of probiotic banana juice on obesity associated complications and hepatosteatosis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Prabhakar Yellanur Konda ◽  
Vijayakumar Poondla ◽  
Krishna Kumar Jaiswal ◽  
Sreenivasulu Dasari ◽  
Reddemma Uyyala ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Liver Lipid ◽  
Normal Liver ◽  
Fat Free Mass ◽  
High Fat ◽  
Fat Percentage ◽  
Liver Size ◽  
Banana Juice ◽  
Study Results ◽  
Enzyme Markers

Abstract The high fat diet alters intestinal microbiota due to increased intestinal permeability and susceptibility to microbial antigens leads to metabolic endotoxemia. But probiotic juices reported for various health benefits. In this background we hypothesized that pectinase treated probiotic banana juice has diverse effects on HFD induced obesity and non-alcoholic steatohepatitis. 20 weeks fed HFD successfully induced obesity and its associated complications in experimental rats. The supplementation of probiotic banana juice for 5 months at a dose of 5 mL/kg bw/day resulted significant decrease (p < 0.05) in body weight (380 ± 0.34), total fat (72 ± 0.8), fat percentage (17 ± 0.07) and fat free mass (165 ± 0.02). Reduction (p < 0.05) in insulin resistance (5.20 ± 0.03), lipid profile (TC 120 ± 0.05; TG 160 ± 0.24; HDL 38 ± 0.03), liver lipid peroxidation (0.7 ± 0.01), hepatic enzyme markers (AST 82 ± 0.06; ALT 78 ± 0.34; ALP 42 ± 0.22), and hepatic steatosis by increasing liver antioxidant potential (CAT 1.4 ± 0.30; GSH 1.04 ± 0.04; SOD 0.82 ± 0.22) with normal hepatic triglycerides (15 ± 0.02) and glycogen (0.022 ± 0.15) contents and also showed normal liver size, less accumulation of lipid droplets with only a few congestion. It is concluded that the increased intestinal S. cerevisiae yeast can switch anti-obesity, antidiabetic, antioxidative stress, antioxidant and anti-hepatosteatosis effect. This study results will have significant implications for treatment of NAFLD.

Abstract 037: Role of Pro-opiomelanocortin (POMC) Specific PTP1B in Differential Regulation of Blood Pressure, Liver Lipid Accumulation and Glucose Tolerance in Response to a High Fat Diet

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Nicola Aberdein ◽  
Jussara M do Carmo ◽  
Zhen Wang ◽  
Taolin Fang ◽  
Cecilia P de Lara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glucose Tolerance ◽  
Fat Mass ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Acute Stress ◽  
Liver Lipid ◽  
Liver Weight ◽  
Metabolic Effects ◽  
High Fat

Obese subjects are often resistant to leptin’s metabolic effects although blood pressure (BP) and sympathetic nervous system responses appear to be preserved. Protein tyrosine phosphatase 1B (PTP1B), a negative regulator of leptin signaling, may play a role in promoting this selective leptin resistance and causing metabolic dysfunction in obesity. Our previous studies suggest that the chronic BP responses to leptin are mediated via activation of pro-opiomelanocortin (POMC) neurons. The goal of this study was to determine if PTP1B in POMC neurons differentially controls metabolic functions and BP in mice fed a high fat diet (HFD). Male mice with POMC specific PTP1B deletion (POMC/PTP1B -/- ) and littermate controls (PTP1B flox/flox ) were fed a HFD from 6 to 22 wks of age. Baseline BP after 16 weeks of a HFD (95±2 vs. 95±3 mmHg) and BP responses to acute stress (Δ32±0 vs. Δ32±6 mmHg), measured by telemetry, were not different in POMC/PTP1B -/- compared to control mice, respectively. Heart rate (HR) was not different in POMC/PTP1B -/- and control mice during acute stress (699±4 vs. 697±15 bpm, respectively). Total body weight (TBW) and fat mass were reduced at 20 weeks of age in POMC/PTP1B -/- compared to controls (36.7±0.1 vs. 42.0±1 g TBW and 12.7±0.4 vs. 16.1±1.0 g fat mass, respectively). Liver weight of POMC/PTP1B -/- mice was less than in controls, and this was evident even when liver weight was normalized as % of TBW (4.5±0.2 vs. 5.0±0.2 %). POMC/PTP1B -/- males had reduced liver lipid accumulation compared to controls as measured by EchoMRI (0.08±0.03 vs. 0.15±0.03 g/g liver weight). Glucose tolerance was also improved by 46% in POMC/PTP1B -/- compared to controls as measured by AUC, 25856±1683 vs. 47267±5616 mg/dLx120min, respectively. These findings indicate that PTP1B signaling in POMC neurons plays a crucial role in regulating liver lipid accumulation and glucose tolerance but does not appear to mediate changes in BP or BP responses to acute stress in mice fed a high HFD (supported by NHLBI-PO1HL51971 and NIGMS P20GM104357)

scholarly journals Molecular adaptation in adipose tissue in response to overfeeding with a high-fat diet under sedentary conditions in South Asian and Caucasian men

2019 ◽  
Vol 122 (03) ◽  
pp. 241-251
Author(s):  
Siti N. Wulan ◽  
Freek G. Bouwman ◽  
Klaas R. Westerterp ◽  
Edwin C. M. Mariman ◽  
Guy Plasqui
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
South Asian ◽  
High Fat Diet ◽  
South Asians ◽  
Molecular Adaptation ◽  
Body Fat Percentage ◽  
High Fat ◽  
Fat Percentage ◽  
Caucasian Men

AbstractFor the same BMI, South Asians have a higher body fat percentage than Caucasians. There might be differences in the fatty acid (FA) handling in adipose tissue when both ethnicities are exposed to high-fat overfeeding. The objective of the present study was to investigate the molecular adaptation in relation to FA metabolism in response to overfeeding with a high-fat diet (OHFD) in South Asian and Caucasian men. Ten South Asian men (BMI 18–29 kg/m2) and ten Caucasian men (BMI 22–33 kg/m2), matched for body fat percentage, aged 20–40 years were included. A weight-maintenance diet (30 % fat, 55 % carbohydrate and 15 % protein) was given for 3 d followed by 3 d of overfeeding (150 % energy requirement) with a high-fat diet (60 % fat, 25 % carbohydrate and 15 % protein) while staying in a respiration chamber. Before and after overfeeding, abdominal subcutaneous fat biopsies were taken. Proteins were isolated, analysed and quantified for short-chain 3-hydroxyacyl-CoA dehydrogenase (HADH), carnitine palmitoyl-transferase 1α (CPT1a), adipose TAG lipase, perilipin A (PLINA), perilipin B, lipoprotein lipase and fatty acid binding protein 4 using Western blotting. OHFD decreased the HADH level (P &lt; 0·05) in Caucasians more than in Asians (P &lt; 0·05), but the baseline and after intervention HADH level was relatively higher in Caucasians. The level of CPT1a decreased in South Asians and increased in Caucasians (P &lt; 0·05). PLINA did not change with diet but the level was higher in South Asians (P &lt; 0·05). The observed differences in HADH and PLINA levels as well as in CPT1a response may be important for differences in the long-term regulation of energy (fat) metabolism in these populations.

scholarly journals Effects of monobutyrin and tributyrin on liver lipid profile, caecal microbiota composition and SCFA in high-fat diet-fed rats

2017 ◽  
Vol 6 ◽  
Author(s):  
Thao Duy Nguyen ◽  
Olena Prykhodko ◽  
Frida Fåk Hållenius ◽  
Margareta Nyman
Keyword(s):  
Succinic Acid ◽  
High Fat Diet ◽  
Intestinal Tract ◽  
Liver Lipid ◽  
Microbiota Composition ◽  
Risk Markers ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets ◽  
Caecal Microbiota

AbstractButyric acid has been shown to have suppressive effects on inflammation and diseases related to the intestinal tract. The aim of the present study was to investigate whether supplementation of two glycerol esters, monobutyrin (MB) and tributyrin (TB), would reach the hindgut of rats, thus having an effect on the caecal profile of SCFA, microbiota composition and some risk markers associated with chronic inflammation. For this purpose, rats were fed high-fat diets after adding MB (1 and 5 g/kg) and TB (5 g/kg) to a diet without any supplementation (high-fat control; HFC). A low-fat (LF) diet was also included. In the liver, total cholesterol concentrations, LDL-cholesterol concentrations, LDL:HDL ratio, and succinic acid concentrations were reduced in rats given the MB and TB (5 g/kg) diets, compared with the group fed the HFC diet. These effects were more pronounced in MB than TB groups as also expressed by down-regulation of the gene Cyp8b1. The composition of the caecal microbiota in rats fed MB and TB was separated from the group fed the HFC diet, and also the LF diet, as evidenced by the absence of the phylum TM7 and reduced abundance of the genera Dorea (similar to LF-fed rats) and rc4-4. Notably, the caecal abundance of Mucispirillum was markedly increased in the MB group compared with the HFC group. The results suggest that dietary supplementation of MB and TB can be used to counteract disturbances associated with a HFC diet, by altering the gut microbiota, and decreasing liver lipids and succinic acid concentrations.

scholarly journals Obesity is Irreversible Without a Controlled Dietary Regimen in a Murine Model

2019 ◽  
Vol 4 (4) ◽  
pp. 2473011419S0040
Author(s):  
Chris Stauch ◽  
Jesse King ◽  
Morgan Kim ◽  
David Waning ◽  
John Elfar ◽  
...  
Keyword(s):  
Body Fat ◽  
High Intensity ◽  
High Fat Diet ◽  
Exercise Program ◽  
Body Fat Percentage ◽  
Obese Mice ◽  
High Fat ◽  
Fat Percentage ◽  
Mineral Density ◽  
Cardiovascular Training

Category: Diabetes, Hindfoot, Midfoot/Forefoot, obesity Introduction/Purpose: In recent decades, the prevalence of obesity in the United States has increased dramatically. This can be attributed in-part to the high-fat “Western Diet”. Consequentially, the economic burden of obesity to the healthcare system has rapidly increased, accounting for more than 10 percent of all medical spending in America. Furthermore, with regards to orthopedics, obesity has been shown to be a strong risk factor for musculoskeletal pain, injury, and post-operative complications. The purpose of this study was to determine the effects of high intensity cardiovascular training and controlled dietary intake on body weight, body fat percentage (BFP), and bone mineral density (BMD) in obese and non-obese mice. These results will provide a better understanding of how to optimally facilitate weight loss in obese patients. Methods: Following IAUCUC approval, 8 diet-induced obesity (DIO) C57BL/6 mice were obtained along with 6 non-obese C57BL/6 control mice. DIO mice were fed a high-fat diet (60% fat by kcal) ad libitum starting at the age of 6 weeks. Control mice were fed a standard low-fat diet (10% fat by kcal) ad libitum from birth. Starting at the age of 14 weeks, all mice underwent a controlled high intensity cardiovascular training protocol using a treadmill four times per week at 30 minute intervals. This was carried out for seven weeks including a one-week acclimation period. Speed, distance, and time spent running were all constant between groups. Mouse body weights were recorded several times per week throughout the study. Additionally, BFP and BMD were obtained bi-weekly using dual energy X-ray absorptiometry (DEXA) to assess morphophysiological changes longitudinally. Results: Preliminary investigations with a controlled exercise regimen reveal that obese mice, when fed a high-fat diet, continue to gain weight rapidly despite high intensity cardiovascular training whereas control mice maintain their weight. Following the seven-week training period, control mice gained an average of 1.25 g (p=0.41), while DIO mice gained an average of 8.55 g (p<0.001). DIO mice also showed an 8.74% increase in body fat percentage (p=0.002) while control mice showed a 0.51% decrease in body fat percentage (p=0.75). Lastly, BMD was significantly lower in DIO mice compared to controls following the exercise protocol (p<0.05). Conclusion: The results of this study support the hypothesis that a controlled exercise regimen alone is ineffective for facilitating weight loss. In fact, obese mice administered a high-fat diet actually gain weight despite undergoing a rigorous exercise program. Additionally, simple differences in dietary intake have significant effects on body weight, body fat percentage, and bone mineral density. This suggests that while exercise may play a small role in maintaining a normal weight, obesity is irreversible with exercise alone. Obese orthopedic patients should be counseled on dietary modifications before engaging in an exercise program.

scholarly journals Regulation of the Body Fat Percentage in Developmental-Stage Rats by Methylxanthine Derivatives in a High-Fat Diet

2006 ◽  
Vol 70 (5) ◽  
pp. 1134-1139 ◽  
Author(s):  
Hiroko INOUE ◽  
Kazuo KOBAYASHI-HATTORI ◽  
Yumi HORIUCHI ◽  
Yuichi OISHI ◽  
Souichi ARAI ◽  
...  
Keyword(s):  
Developmental Stage ◽  
Body Fat ◽  
High Fat Diet ◽  
The Body ◽  
Body Fat Percentage ◽  
High Fat ◽  
Fat Percentage

Transgenic MSH overexpression attenuates the metabolic effects of a high-fat diet

2007 ◽  
Vol 293 (1) ◽  
pp. E121-E131 ◽  
Author(s):  
Michelle Lee ◽  
Andrea Kim ◽  
Streamson C. Chua ◽  
Silvana Obici ◽  
Sharon L. Wardlaw
Keyword(s):  
High Fat Diet ◽  
Metabolic Effects ◽  
High Fat ◽  
Fat Percentage ◽  
Male And Female ◽  
Fat Accumulation ◽  
Low Fat Diet ◽  
Hepatic Fat ◽  
Biochemical Analyses

To determine whether long-term melanocortinergic activation can attenuate the metabolic effects of a high fat diet, mice overexpressing an NH2-terminal POMC transgene that includes α- and γ3-MSH were studied on either a 10% low-fat diet (LFD) or 45% high-fat diet (HFD). Weight gain was modestly reduced in transgenic (Tg-MSH) male and female mice vs. wild type (WT) on HFD ( P < 0.05) but not LFD. Substantial reductions in body fat percentage were found in both male and female Tg-MSH mice on LFD ( P < 0.05) and were more pronounced on HFD ( P < 0.001). These changes occurred in the absence of significant feeding differences in most groups, consistent with effects of Tg-MSH on energy expenditure and partitioning. This is supported by indirect calorimetry studies demonstrating higher resting oxygen consumption and lower RQ in Tg-MSH mice on the HFD. Tg-MSH mice had lower fasting insulin levels and improved glucose tolerance on both diets. Histological and biochemical analyses revealed that hepatic fat accumulation was markedly reduced in Tg-MSH mice on the HFD. Tg-MSH also attenuated the increase in corticosterone induced by the HFD. Higher levels of Agrp mRNA, which might counteract effects of the transgene, were measured in Tg-MSH mice on LFD ( P = 0.02) but not HFD. These data show that long-term melanocortin activation reduces body weight, adiposity, and hepatic fat accumulation and improves glucose metabolism, particularly in the setting of diet-induced obesity. Our results suggest that long-term melanocortinergic activation could serve as a potential strategy for the treatment of obesity and its deleterious metabolic consequences.

scholarly journals Palm Oil and Egusi Melon Oil Lower Serum and Liver Lipid Profile and Improve Antioxidant Activity in Rats Fed a High Fat Diet

2010 ◽  
Vol 8 (4) ◽  
pp. 154-158
Author(s):  
George O. Eidangbe ◽  
Godwin C. Ojieh ◽  
Blessing O. Idonije ◽  
Olarewaju M. Oluba
Keyword(s):  
Antioxidant Activity ◽  
Lipid Profile ◽  
Palm Oil ◽  
High Fat Diet ◽  
Liver Lipid ◽  
High Fat ◽  
Lower Serum

scholarly journals Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260546
Author(s):  
Mary J. Obayemi ◽  
Christopher O. Akintayo ◽  
Adesola A. Oniyide ◽  
Ayodeji Aturamu ◽  
Olabimpe C. Badejogbin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Food Intake ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Liver Lipid ◽  
Control Group ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Male Wistar Rats

Background Adipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats. Materials and methods Twenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks. Results HFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin. Conclusion Taken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.

scholarly journals Integrated Transcriptomic and Translatomic Inquiry of the Role of Betaine on Lipid Metabolic Dysregulation Induced by a High-Fat Diet

2021 ◽  
Vol 8 ◽  
Author(s):  
Tengda Huang ◽  
Lin Yu ◽  
Hongyuan Pan ◽  
Zeqiang Ma ◽  
Tian Wu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Liver Lipid ◽  
Liver Steatosis ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Translational Efficiency ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Translational Level

An excessive high-fat/energy diet is a major cause of obesity and linked complications, such as non-alcoholic fatty liver disease (NAFLD). Betaine has been shown to effectively improve hepatic lipid metabolism. However, the mechanistic basis for this improvement is largely unknown. Herein, integration of mRNA sequencing and ribosome footprints profiling (Ribo-seq) was used to investigate the means by which betaine alleviates liver lipid metabolic disorders induced by a high-fat diet. For the transcriptome, gene set enrichment analysis demonstrated betaine to reduce liver steatosis by up-regulation of fatty acid beta oxidation, lipid oxidation, and fatty acid catabolic processes. For the translatome, 574 differentially expressed genes were identified, 17 of which were associated with the NAFLD pathway. By combined analysis of transcriptome and translatome, we found that betaine had the greater effect on NAFLD at the translational level. Further, betaine decreased translational efficiency (TE) for IDI1, CYP51A1, TM7SF2, and APOA4, which are related to lipid biosynthesis. In summary, this study demonstrated betaine alleviating lipid metabolic dysfunction at the translational level. The transcriptome and translatome data integration approach used herein provides for a new understanding of the means by which to treat NAFLD.

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