Search Results

You are looking at 1 - 10 of 49 items for :

  • "adipocyte hypertrophy" x
Clear All
Free access

Eun Hee Koh, Ah-Ram Kim, Hyunshik Kim, Jin Hee Kim, Hye-Sun Park, Myoung Seok Ko, Mi-Ok Kim, Hyuk-Joong Kim, Bum Joong Kim, Hyun Ju Yoo, Su Jung Kim, Jin Sun Oh, Chang-Yun Woo, Jung Eun Jang, Jaechan Leem, Myung Hwan Cho and Ki-Up Lee

include adipose tissue hypoxia ( Ye et al . 2007 , Jiang et al . 2011 ), increased proinflammatory cytokine levels, and oxidative stress in dysfunctional adipocytes ( Otani 2011 ). Another hypothesis that links adipocyte hypertrophy to reduced

Free access

Renato Simões Gaspar, Renata Ohana Alves Benevides, João Lucas de Lima Fontelles, Caroline Castro Vale, Lucas Martins França, Paulo de Tarso Silva Barros and Antonio Marcus de Andrade Paes

exhibited obesity, hypertriglyceridemia, and visceral adipocyte hypertrophy. Additionally, they had irregular estrous cycles, with oligo-ovulation, and increased number of ovarian follicular cysts and atretic follicles. Moreover, our MSG rats presented

Free access

Anthony M Belenchia, Sarah A Johnson, Mark R Ellersieck, Cheryl S Rosenfeld and Catherine A Peterson

-low fat (VDS-LF), vitamin D sufficient-high fat (VDS-HF), vitamin D deficient-low fat (VDD-LF) and vitamin D deficient-high fat (VDD-HF) offspring groups, respectively. Arrows indicate larger adipocytes (hypertrophied) compared to the mean of the VDS

Restricted access

Akiko Mizokami, Satoru Mukai, Jing Gao, Tomoyo Kawakubo-Yasukochi, Takahito Otani, Hiroshi Takeuchi, Eijiro Jimi and Masato Hirata

, insulin resistance, and adipocyte hypertrophy, likely as a result of the promotion of gluconeogenesis in the liver and inflammation in adipose tissue. Our results thus indicate that GLP-1R signaling is necessary for the beneficial actions of GluOC and that

Free access

Elaine de Oliveira, Egberto G Moura, Ana Paula Santos-Silva, Cíntia R Pinheiro, Natalia S Lima, José Firmino Nogueira-Neto, Andre L Nunes-Freitas, Yael Abreu-Villaça, Magna C F Passos and Patrícia C Lisboa

offspring was associated with an increase in the size of adipocytes (hypertrophy), we performed morphometric analysis on histological sections of visceral and subcutaneous adipose tissue ( Fig. 3 A and B). Quantitative analysis of these sections showed that

Free access

Simon Lecoutre, Barbara Deracinois, Christine Laborie, Delphine Eberlé, Céline Guinez, Polina E Panchenko, Jean Lesage, Didier Vieau, Claudine Junien, Anne Gabory and Christophe Breton

-lasting consequences on visceral WAT of adult rat offspring in a depot- and sex-specific manner. In particular, we showed that HF adult male offspring exhibit greater visceral fat pad weights with adipocyte hypertrophy and hyperplasia, despite no difference in BW and

Restricted access

Ali Aflatounian, Melissa C Edwards, Valentina Rodriguez Paris, Michael J Bertoldo, Reena Desai, Robert B Gilchrist, William L Ledger, David J Handelsman and Kirsty A Walters

As the mechanistic basis of polycystic ovary syndrome (PCOS) remains unknown, current management relies on symptomatic treatment. Hyperandrogenism is a major PCOS characteristic and evidence supports it playing a key role in PCOS pathogenesis. Classically androgens can act directly through the androgen receptor (AR), or indirectly, following aromatization, via the estrogen receptor (ER). We investigated the mechanism of androgenic actions driving PCOS by comparing the capacity of non-aromatizable dihydrotestosterone (DHT) and aromatizable testosterone to induce PCOS traits in wildtype (WT) and AR-knockout (ARKO) mice. DHT and testosterone induced the reproductive PCOS-like features of acyclicity and anovulation in WT females. In ARKO mice DHT did not cause reproductive dysfunction, however testosterone treatment induced irregular cycles and ovulatory disruption. These findings indicate that direct AR actions and indirect, likely ER actions, are important mediators of PCOS reproductive traits. DHT, but not testosterone, induced an increase in body weight, body fat, serum cholesterol and adipocyte hypertrophy in WT mice, but neither androgen induced these metabolic features in ARKO mice. These data infer that direct AR-driven mechanisms are key in driving the development of PCOS metabolic traits. Overall, these findings demonstrate that differing PCOS traits can be mediated via different steroid signaling pathways and indicate that a phenotype-based treatment approach would ensure effective targeting of the underlying mechanisms.

Restricted access

Catalina Sierra-Ramos, Silvia Velazquez-Garcia, Arianna Vastola-Mascolo, Guadalberto Hernández, Nourdine Faresse and Diego Alvarez de la Rosa

)-induced model of obesity and glucose intolerance. Our results demonstrated exacerbated body weight gain due to fat accumulation, adipocyte hypertrophy, dyslipidemia and hyperinsulinemia, prominent glucose and insulin intolerance and a rapid development of

Free access

Nailliw Z Preite, Bruna P P do Nascimento, Cynthia R Muller, Anna Laura V Américo, Talita S Higa, Fabiana S Evangelista, Carmen L Lancellotti, Felipe dos Santos Henriques, Miguel Luiz Batista Jr, Antonio C Bianco and Miriam O Ribeiro

) of 24.5-fold ( P  > 0.01) when compared with controls (ARβ 3 KO). HFD also induced adipocyte hypertrophy in WT (6.9-fold, P  > 0.01), compared with WT controls. The adipocyte hypertrophy was 1.6-fold higher in ARβ 3 KO group when compared with WT

Restricted access

Guillermo García-Eguren, Oriol Giró, María del Mar Romero, Mar Grasa and Felicia A Hanzu

, both treatments induced similar levels of adipocyte hypertrophy ( Fig. 5B and C ) and showed the same adipocyte size distribution pattern at the end of treatment ( Fig. 5D ). After the recovery period, the HFD-treated group decreased adipocyte area