scholarly journals Loss of Monoacylglycerol O-Acyltransferase 2 can be Compensated for by Diacylglycerol O-Acyltransferases 1 and 2 in High-Fat Diet-Induced Obesity and Mammary Cancer Development

2021 ◽  
Author(s):  
Yan Mei ◽  
Jing Wang ◽  
Jia-Bin Lu ◽  
Guan-Ming Lu ◽  
Li-Xia Peng ◽  
...  
Keyword(s):  
Overall Survival ◽  
Mammary Tumor ◽  
High Fat Diet ◽  
Triple Negative ◽  
Tumor Development ◽  
Breast Adenocarcinoma ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Increased Risk ◽  
Deficient Mice

Abstract Background: Dietary fat absorption involves the re-esterification of digested triacylglycerol in the enterocytes, it is a biological process catalyzed by monoacylglycerol O-acyltransferase 2 (MOGAT2, aka MGAT2), which is highly expressed in the small intestine. A previous study showed that the loss of the Mogat2 gene can prevent high-fat diet-induced obesity in mice. Obesity is associated with an increased risk of several types of cancer including postmenopausal breast cancer.Methods: We collected 147 patients with triple negative breast adenocarcinoma to explore the relationship between the expression of MOGAT2 and patient overall survival. And we generated a Mogat2-deficient mouse mammary tumor model by crossing Mogat2-deficient mice with MMTV-PyMT mice to examine the effect of losing MOGAT2 in vivo.Results: Our founding suggest that obesity was induced by a relatively high-fat diet (37% of calories from fat) in the mice with or without Mogat2 knockout. Mammary tumor development was deteriorated by a relatively high-fat diet regardless of Mogat2 deficiency. As a compensation mechanism, upregulation of diacylglycerol O-acyltransferases 1 and 2 (Dgat1 and Dgat2) in the Mogat2 deficient mice was found. Conclusions: Elevated expression of MOGAT2 in triple negative breast adenocarcinoma predicts poorer patient overall survival. With the compensation of Dgat1 and Dgat2, Mogat2 deficiency alone cannot prevent fat diet-induced obesity, nor prevent mammary tumor development in a mouse model.

scholarly journals Loss of Monoacylglycerol O Acyltransferase 2 Can Be Compensated for by Diacylglycerol O Acyltransferases 1 and 2 in High Fat Diet Induced Obesity and Mammary Cancer Development

2021 ◽  
Author(s):  
Yan Mei ◽  
Jing Wang ◽  
Jia-Bin Lu ◽  
Guan-Ming Lu ◽  
Li-Xia Peng ◽  
...  
Keyword(s):  
Overall Survival ◽  
Mammary Tumor ◽  
High Fat Diet ◽  
Triple Negative ◽  
Tumor Development ◽  
Breast Adenocarcinoma ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Increased Risk ◽  
Deficient Mice

Abstract Background: Dietary fat absorption involves the re esterification of digested triacylglycerol in the enterocytes, it is a biological process catalyzed by monoacylglycerol O acyltransferase 2 (MOGAT2, aka MGAT2), which is highly expressed in the small intestine. A previous study showed that the loss of the Mogat2 gene can prevent high fat diet induced obesity in mice. Obesity is associated with an increased risk of several types of cancer including postmenopausal breast cancer.Methods: We collected 147 patients with triple negative breast adenocarcinoma to explore the relationship between the expression of MOGAT2 and patient overall survival. And we generated a Mogat2 deficient mouse mammary tumor model by crossing Mogat2 deficient mice with MMTV PyMT mice to examine the effect of losing MOGAT2 in vivo. Results: Our founding suggest that obesity was induced by a relatively high fat diet (37% of calories from fat) in the mice with or without Mogat2 knockout. Mammary tumor development was deteriorated by a relatively high fat diet regardless of Mogat2 deficiency. As a compensation mechanism, upregulation of diacylglycerol O acyltransferases 1 and 2 (Dgat1 and Dgat2) in the Mogat2 deficient mice was found. Conclusions: Elevated expression of MOGAT2 in triple negative breast adenocarcinoma predicts poorer patient overall survival. With the compensation of Dgat1 and Dgat2, Mogat2 deficiency alone cannot prevent fat diet induced obesity, nor prevent mammary tumor development in a mouse model.

Klotho-Deficient Mice Are Resistant to High-Fat Diet-Induced Obesity

2011 ◽  
pp. P3-368-P3-368
Author(s):  
Junko Akiyoshi ◽  
Mutsuko Ohnishi ◽  
Shigeko Kato ◽  
Khadijah Turkistani ◽  
Azeddine Atfi ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Deficient Mice

scholarly journals Estradiol and high fat diet associate with changes in gut microbiota in female ob/ob mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kalpana D. Acharya ◽  
Xing Gao ◽  
Elizabeth P. Bless ◽  
Jun Chen ◽  
Marc J. Tetel
Keyword(s):  
Weight Gain ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Low Grade ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Increased Risk ◽  
17Β Estradiol ◽  
Low Grade Inflammation

AbstractEstrogens protect against diet-induced obesity in women and female rodents. For example, a lack of estrogens in postmenopausal women is associated with an increased risk of weight gain, cardiovascular diseases, low-grade inflammation, and cancer. Estrogens act with leptin to regulate energy homeostasis in females. Leptin-deficient mice (ob/ob) exhibit morbid obesity and insulin resistance. The gut microbiome is also critical in regulating metabolism. The present study investigates whether estrogens and leptin modulate gut microbiota in ovariectomized ob/ob (obese) or heterozygote (lean) mice fed high-fat diet (HFD) that received either 17β-Estradiol (E2) or vehicle implants. E2 attenuated weight gain in both genotypes. Moreover, both obesity (ob/ob mice) and E2 were associated with reduced gut microbial diversity. ob/ob mice exhibited lower species richness than control mice, while E2-treated mice had reduced evenness compared with vehicle mice. Regarding taxa, E2 was associated with an increased abundance of the S24-7 family, while leptin was associated with increases in Coriobacteriaceae, Clostridium and Lactobacillus. Some taxa were affected by both E2 and leptin, suggesting these hormones alter gut microbiota of HFD-fed female mice. Understanding the role of E2 and leptin in regulating gut microbiota will provide important insights into hormone-dependent metabolic disorders in women.

Effects of Soy-Derived Isoflavones and a High-Fat Diet on Spontaneous Mammary Tumor Development in Tg.NK (MMTV/c-neu) Mice

2004 ◽  
Vol 50 (1) ◽  
pp. 46-54 ◽  
Author(s):  
Mirjam Luijten ◽  
Anni Ronfeldt Thomsen ◽  
Jolanda A. H. van den Berg ◽  
Piet W. Wester ◽  
Aart Verhoef ◽  
...  
Keyword(s):  
Mammary Tumor ◽  
High Fat Diet ◽  
Tumor Development ◽  
High Fat ◽  
Spontaneous Mammary Tumor

scholarly journals The Molecular Effects of a High Fat Diet on Endometrial Tumour Biology

Life ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 188
Author(s):  
Michael Wilkinson ◽  
Piriyah Sinclair ◽  
Ludmilla Dellatorre-Teixeira ◽  
Patrick Swan ◽  
Eoin Brennan ◽  
...  
Keyword(s):  
Overall Survival ◽  
Endometrial Cancer ◽  
Weight Gain ◽  
Rat Model ◽  
High Fat Diet ◽  
Cancer Metastasis ◽  
Chow Diet ◽  
Suitable Model ◽  
High Fat ◽  
Diet Induced Obesity

We sought to validate the BDII/Han rat model as a model for diet-induced obesity in endometrial cancer (EC) and determine if transcriptomic changes induced by a high fat diet (HFD) in an EC rat model can be used to identify novel biomarkers in human EC. Nineteen BDII/Han rats were included. Group A (n = 7) were given ad lib access to a normal calorie, normal chow diet (NCD) while Group B (n = 12) were given ad lib access to a calorie rich HFD for 15 months. RNAseq was performed on endometrial tumours from both groups. The top-ranking differentially expressed genes (DEGs) were examined in the human EC using The Cancer Genome Atlas (TCGA) to assess if the BDII/Han rat model is an appropriate model for human obesity-induced carcinogenesis. Weight gain in HFD rats was double the weight gain of NCD rats (50 g vs. 25 g). The incidence of cancer was similar in both groups (4/7—57% vs. 4/12—33%; p = 0.37). All tumours were equivalent to a Stage 1A, Grade 2 human endometrioid carcinoma. A total of 368 DEGs were identified between the tumours in the HFD group compared to the NCD group. We identified two upstream regulators of the DEGs, mir-33 and Brd4, and a pathway analysis identified downstream enrichment of the colorectal cancer metastasis and ovarian cancer metastasis pathways. Top-ranking DEGs included Tex14, A2M, Hmgcs2, Adamts5, Pdk4, Crabp2, Capn12, Npw, Idi1 and Gpt. A2M expression was decreased in HFD tumours. Consistent with these findings, we found a significant negative correlation between A2M mRNA expression levels and BMI in the TCGA cohort (Spearman’s Rho = −0.263, p < 0.001). A2M expression was associated with improved overall survival (HR = 0.45, 95% CI 0.23–0.9, p = 0.024). Crabp2 expression was increased in HFD tumours. In human EC, CRABP2 expression was associated with reduced overall survival (HR = 3.554, 95% CI 1.875–6.753, p < 0.001). Diet-induced obesity can alter EC transcriptomic profiles. The BDII/Han rat model is a suitable model of diet-induced obesity in endometrial cancer and can be used to identify clinically relevant biomarkers in human EC.

scholarly journals Casitas b-Lineage Lymphoma-Deficient Mice Are Protected Against High-Fat Diet-Induced Obesity and Insulin Resistance

Diabetes ◽  
2006 ◽  
Vol 55 (3) ◽  
pp. 708-715 ◽  
Author(s):  
J. C. Molero ◽  
S. G. Waring ◽  
A. Cooper ◽  
N. Turner ◽  
R. Laybutt ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
B Lineage ◽  
Deficient Mice

scholarly journals Autophagy-mediated metabolic effects of aspirin

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Francesca Castoldi ◽  
Juliette Humeau ◽  
Isabelle Martins ◽  
Sylvie Lachkar ◽  
Damarys Loew ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Effects ◽  
Tumor Control ◽  
Protein Acetylation ◽  
High Fat ◽  
Blood Leukocytes ◽  
Diet Induced Obesity ◽  
Autophagy Gene ◽  
General Protein ◽  
Deficient Mice

AbstractSalicylate, the active derivative of aspirin (acetylsalicylate), recapitulates the mode of action of caloric restriction inasmuch as it stimulates autophagy through the inhibition of the acetyltransferase activity of EP300. Here, we directly compared the metabolic effects of aspirin medication with those elicited by 48 h fasting in mice, revealing convergent alterations in the plasma and the heart metabolome. Aspirin caused a transient reduction of general protein acetylation in blood leukocytes, accompanied by the induction of autophagy. However, these effects on global protein acetylation could not be attributed to the mere inhibition of EP300, as determined by epistatic experiments and exploration of the acetyl-proteome from salicylate-treated EP300-deficient cells. Aspirin reduced high-fat diet-induced obesity, diabetes, and hepatosteatosis. These aspirin effects were observed in autophagy-competent mice but not in two different models of genetic (Atg4b−/− or Bcln1+/−) autophagy-deficiency. Aspirin also improved tumor control by immunogenic chemotherapeutics, and this effect was lost in T cell-deficient mice, as well as upon knockdown of an essential autophagy gene (Atg5) in cancer cells. Hence, the health-improving effects of aspirin depend on autophagy.

Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

1994 ◽  
Vol 71 (06) ◽  
pp. 755-758 ◽  
Author(s):  
E M Bladbjerg ◽  
P Marckmann ◽  
B Sandström ◽  
J Jespersen
Keyword(s):  
High Fat Diet ◽  
Fat Content ◽  
Factor Vii ◽  
Amidolytic Activity ◽  
High Fat ◽  
Low Fat Diet ◽  
Increased Risk ◽  
Coagulant Activity ◽  
High Fat Diets ◽  
Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

Glucagon under high fat diet induced obesity

2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
LC Bollheimer ◽  
H Wobser ◽  
CE Wrede ◽  
A Schäffler ◽  
J Schölmerich ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity
Sign in / Sign up

Export Citation Format

Share Document