Dietary trimethylamine N-oxide exacerbates impaired glucose tolerance in mice fed a high fat diet

2014 ◽  
Vol 118 (4) ◽  
pp. 476-481 ◽  
Author(s):  
Xiang Gao ◽  
Xiaofang Liu ◽  
Jie Xu ◽  
Changhu Xue ◽  
Yong Xue ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
High Fat

scholarly journals Adult offspring of high-fat diet-fed dams can have normal glucose tolerance and body composition

2014 ◽  
Vol 5 (3) ◽  
pp. 229-239 ◽  
Author(s):  
K. M. Platt ◽  
R. J. Charnigo ◽  
K. J. Pearson
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
High Fat ◽  
High Fat Diets ◽  
Normal Glucose ◽  
Fat Diets

Maternal high-fat diet consumption and obesity have been shown to program long-term obesity and lead to impaired glucose tolerance in offspring. Many rodent studies, however, use non-purified, cereal-based diets as the control for purified high-fat diets. In this study, primiparous ICR mice were fed purified control diet (10–11 kcal% from fat of lard or butter origin) and lard (45 or 60 kcal% fat) or butter (32 or 60 kcal% fat)-based high-fat diets for 4 weeks before mating, throughout pregnancy, and for 2 weeks of nursing. Before mating, female mice fed the 32 and 60% butter-based high-fat diets exhibited impaired glucose tolerance but those females fed the lard-based diets showed normal glucose disposal following a glucose challenge. High-fat diet consumption by female mice of all groups decreased lean to fat mass ratios during the 4th week of diet treatment compared with those mice consuming the 10–11% fat diets. All females were bred to male mice and pregnancy and offspring outcomes were monitored. The body weight of pups born to 45% lard-fed dams was significantly increased before weaning, but only female offspring born to 32% butter-fed dams exhibited long-term body weight increases. Offspring glucose tolerance and body composition were measured for at least 1 year. Minimal, if any, differences were observed in the offspring parameters. These results suggest that many variables should be considered when designing future high-fat diet feeding and maternal obesity studies in mice.

Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice

2015 ◽  
Vol 6 (4) ◽  
pp. 1117-1125 ◽  
Author(s):  
Xiang Gao ◽  
Jie Xu ◽  
Chengzi Jiang ◽  
Yi Zhang ◽  
Yong Xue ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Fish Oil ◽  
Impaired Glucose Tolerance ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
High Fat ◽  
Dietary Fish

Dietary fish oil could ameliorate trimethylamineN-oxide (TMAO)-induced impaired glucose tolerance in HFD-fed mice.

scholarly journals TRAIL reduces impaired glucose tolerance and NAFLD in the high-fat diet fed mouse

2018 ◽  
Vol 132 (1) ◽  
pp. 69-83 ◽  
Author(s):  
Stella Bernardi ◽  
Barbara Toffoli ◽  
Veronica Tisato ◽  
Fleur Bossi ◽  
Stefania Biffi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
Disease Onset ◽  
High Fat ◽  
Primary Hepatocytes

Recent studies suggest that a circulating protein called TRAIL (TNF-related apoptosis inducing ligand) may have an important role in the treatment of type 2 diabetes. It has been shown that TRAIL deficiency worsens diabetes and that TRAIL delivery, when it is given before disease onset, slows down its development. The present study aimed at evaluating whether TRAIL had the potential not only to prevent, but also to treat type 2 diabetes. Thirty male C57BL/6J mice were randomized to a standard or a high-fat diet (HFD). After 4 weeks of HFD, mice were further randomized to receive either placebo or TRAIL, which was delivered weekly for 8 weeks. Body weight, food intake, fasting glucose, and insulin were measured at baseline and every 4 weeks. Tolerance tests were performed before drug randomization and at the end of the study. Tissues were collected for further analyses. Parallel in vitro studies were conducted on HepG2 cells and mouse primary hepatocytes. TRAIL significantly reduced body weight, adipocyte hypertrophy, free fatty acid levels, and inflammation. Moreover, it significantly improved impaired glucose tolerance, and ameliorated non-alcoholic fatty liver disease (NAFLD). TRAIL treatment reduced liver fat content by 47% in vivo as well as by 45% in HepG2 cells and by 39% in primary hepatocytes. This was associated with a significant increase in liver peroxisome proliferator-activated receptor (PPAR) γ (PPARγ) co-activator-1 α (PGC-1α) expression both in vivo and in vitro, pointing to a direct protective effect of TRAIL on the liver. The present study confirms the ability of TRAIL to significantly attenuate diet-induced metabolic abnormalities, and it shows for the first time that TRAIL is effective also when administered after disease onset. In addition, our data shed light on TRAIL therapeutic potential not only against impaired glucose tolerance, but also against NAFLD.

Collaborative Cross Mouse Population for Studying Alveolar Bone Changes and Impaired Glucose Tolerance Comorbidity After High-Fat Diet Consumption

2017 ◽  
Vol 88 (9) ◽  
pp. e150-e158 ◽  
Author(s):  
Aysar Nashef ◽  
Hanifa J. Abu-Toamih Atamni ◽  
Yuval Buchnik ◽  
Hatice Hasturk ◽  
Alpdogan Kantarci ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
Alveolar Bone ◽  
Collaborative Cross ◽  
High Fat ◽  
Mouse Population ◽  
Bone Changes

scholarly journals Impaired Glucose Tolerance is Associated with Enhanced Platelet-Monocyte Aggregation in Short-Term High-Fat Diet-Fed Mice

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2695 ◽  
Author(s):  
Zibusiso Mkandla ◽  
Tinashe Mutize ◽  
Phiwayinkosi V. Dludla ◽  
Bongani B. Nkambule
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
Hypercoagulable State ◽  
Current Evidence ◽  
High Fat ◽  
Short Term ◽  
Prediabetic State ◽  
Metabolic Dysregulation ◽  
Body Weights

High-fat diet (HFD) feeding is known to induce metabolic dysregulation, however, less is known on its impact in promoting the hypercoagulable state. This current study aimed to evaluate platelet-monocyte aggregate (PMA) formation following short-term HFD feeding. This is particularly important for understanding the link between inflammation and the hypercoagulable state during the early onset of metabolic dysregulation. To explore such a hypothesis, mice were fed a HFD for 8 weeks, with body weights as well as insulin and blood glucose levels monitored on a weekly basis during this period. Basal hematological measurements were determined and the levels of spontaneous peripheral blood PMAs were assessed using whole blood flow cytometry. The results showed that although there were no significant differences in body weights, mice on HFD displayed impaired glucose tolerance and markedly raised insulin levels. These metabolic abnormalities were accompanied by elevated baseline PMA levels as an indication of hypercoagulation. Importantly, it was evident that baseline levels of monocytes, measured using the CD14 monocyte marker, were significantly decreased in HFD-fed mice when compared to controls. In summary, the current evidence shows that in addition to causing glucose intolerance, such as that identified in a prediabetic state, HFD-feeding can promote undesirable hypercoagulation, the major consequence implicated in the development of cardiovascular complications.

scholarly journals Effect of Treatment of Sprague Dawley Rats with AVE7688, Enalapril, or Candoxatril on Diet-Induced Obesity

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Eric P. Davidson ◽  
Lawrence J. Coppey ◽  
Brian Dake ◽  
Mark A. Yorek
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
Sensory Nerve ◽  
Sensory Neuropathy ◽  
Neutral Endopeptidase ◽  
Sprague Dawley ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats

The objective of this study was to determine the effect of AVE7688, a drug that inhibits both angiotensin converting enzyme (ACE) and neutral endopeptidase (NEP) activity, on neural and vascular defects caused by diet induced obesity (DIO). Rats at 12 weeks of age were fed a standard or high fat diet with or without AVE7688 for 24 weeks. DIO rats had impaired glucose tolerance and developed sensory neuropathy. Vascular relaxation to acetylcholine and calcitonin gene-related peptide was decreased in epineurial arterioles of DIO rats. Rats fed a high fat diet containing AVE7688 did not become obese and vascular and sensory nerve dysfunction and impaired glucose tolerance were improved. DIO is associated with increased expression of NEP in epineurial arterioles. NEP degrades vasoactive peptides which may explain the decrease in neurovascular function in DIO.

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