Body composition and hormonal effects following exposure to mycotoxin deoxynivalenol in the high‐fat diet‐induced obese mouse

Kobayashi‐Hattori, Kazuo; Amuzie, Chidozie; Flannery, Brenna M.; Pestka, James J.

doi:10.1002/mnfr.201000640

Cited by 21 publications

(12 citation statements)

References 35 publications

(51 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One factor that may likely contribute to the relative maintenance of metabolic function in pHF mice is the increase in lean mass, which was not observed in aHF mice. These findings are consistent with previous reports, which used NMR to examine body composition in HF-fed mice and reported a pronounced increase in lean mass in pHF compared with LF-or chow-fed controls (34), whereas studies that began HF feeding in adult mice reported little or no change in lean mass (18). Given the primary role of muscle in whole body energy utilization (12), an increase in total lean mass might serve a protective role in maintaining glucose homeostasis to counterbalance the negative impact of fat accumulation.…”

Section: Discussionsupporting

confidence: 94%

Peripubertal-onset but not adult-onset obesity increases IGF-I and drives development of lean mass, which may lessen the metabolic impairment in adult obesity

Córdoba-Chacón

Gahete

Pozo-Salas

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

It has been suggested that adult metabolic dysfunction may be more severe in individuals who become obese as children compared with those who become obese later in life. To determine whether adult metabolic function differs if diet-induced weight gain occurs during the peripubertal age vs. if excess weight gain occurs after puberty, male C57Bl/6J mice were fed a low-fat (LF; 10% kcal from fat) or high-fat (HF; 60% kcal from fat) diet starting during the peripubertal period (pHF; 4 wk of age) or as adults (aHF; 12 wk of age). Both pHF and aHF mice were hyperinsulinemic and hyperglycemic, and both showed impaired glucose tolerance and insulin resistance compared with their LF-fed controls. However, despite a longer time on diet, pHF mice were relatively more insulin sensitive than aHF mice, which was associated with higher lean mass and circulating IGF-I levels. In addition, HF feeding had an overall stimulatory effect on circulating corticosterone levels; however, this rise was associated only with elevated plasma ACTH in the aHF mice. Despite the belief that adult metabolic dysfunction may be more severe in individuals who become obese as children, data generated using a diet-induced obese mouse model suggest that adult metabolic dysfunction associated with peripubertal onset of obesity is not worse than that associated with adult-onset obesity.

show abstract

Section: Discussionsupporting

confidence: 94%

Peripubertal-onset but not adult-onset obesity increases IGF-I and drives development of lean mass, which may lessen the metabolic impairment in adult obesity

Córdoba-Chacón

Gahete

Pozo-Salas

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

“…[27] There is no information about effect of T-2 toxin and HT-2 toxin in combination with leptin on secretion activity of ovarian cells to produce steroid hormones. Kobayashi-Hattori et al [28] observed that DON which is B-trichothecene mycotoxin reduces plasma insulin, leptin, IGF-I, and insulin-like growth factor acid labile subunit as well as increased hypothalamic mRNA level of the orexigenic agouti-related protein.…”

Section: Discussionmentioning

confidence: 98%

Assessment of T-2 toxin effect and its metabolite HT-2 toxin combined with insulin-like growth factor I, leptin and ghrelin on progesterone secretion by rabbit ovarian fragments

Maruniaková

Kádasi

Sirotkin

et al. 2015

Journal of Environmental Science and Health, Part B

View full text Add to dashboard Cite

Assessment of A-trichothecene mycotoxins (T-2 and HT-2 toxins) effect combined with growth factor IGF-I, and the metabolic hormones leptin and ghrelin on progesterone secretion by rabbit ovarian fragments was studied. Rabbit ovarian fragments were incubated without (control group) or with T-2/HT-2 toxin, or their combinations with insulin-like growth factor I (IGF-I), leptin or ghrelin at various concentrations for 24 h. Secretion of progesterone was determined by ELISA. First, T-2 toxin and HT-2 toxins at all doses used (0.01, 0.1, 1, 10, and 100 ng mL(-1)) were not shown to be potential regulators of progesterone secretion in rabbit ovarian fragments. Second, T-2 toxin but not HT-2 toxin combined with IGF-I was shown to be potential regulator of progesterone secretion in rabbit ovarian fragments. T-2 toxin at all doses used (0.01; 0.1; 1; 10; and 100 ng mL(-1)) combined with IGF-I (at dose 100 ng mL(-1)) significantly (P < 0.05) decreased progesterone secretion by rabbit ovarian fragments. Third, T-2 toxin and HT-2 toxin at all doses used in the study (0.01, 0.1, 1, 10, and 100 ng mL(-1)) combined with leptin (at dose 1000 ng mL(-1)) were not shown to be potential regulators of progesterone secretion in rabbit ovarian fragments. Furthermore, T-2 toxin and HT-2 toxin at all doses used in the study (0.01, 0.1, 1, 10, and 100 ng mL(-1)) combined with ghrelin (500 ng mL(-1)) were not shown to be potential regulators of progesterone secretion in rabbit ovarian fragments. Results in this study showed that trichothecene as T-2 toxin combined with IGF-I but not HT-2 toxin was able to decrease progesterone secretion in rabbit ovarian fragments in vitro. Experimental results of T-2 and HT-2 toxins combined with leptin and ghrelin did not confirm ability to modulate progesterone secretion by ovarian fragments in rabbits.

show abstract

“…Recently, a noticeable effort was made to describe more precisely the DON-induced anorexia using mice as a model [19,20,21,22,23]. While swine was reported to be the most sensitive species to DON, numerous in vivo and in vitro DON toxicity studies were conducted on rodents and especially on mice which can be considered as a good model for the study of DON toxicity.…”

Section: Don-induced Anorexia In Mice Modelsmentioning

confidence: 99%

Advances in Deoxynivalenol Toxicity Mechanisms: The Brain as a Target

Bonnet¹,

Roux²,

Mounien³

et al. 2012

Toxins

View full text Add to dashboard Cite

Deoxynivalenol (DON), mainly produced by Fusarium fungi, and also commonly called vomitoxin, is a trichothecene mycotoxin. It is one of the most abundant trichothecenes which contaminate cereals consumed by farm animals and humans. The extent of cereal contamination is strongly associated with rainfall and moisture at the time of flowering and with grain storage conditions. DON consumption may result in intoxication, the severity of which is dose-dependent and may lead to different symptoms including anorexia, vomiting, reduced weight gain, neuroendocrine changes, immunological effects, diarrhea, leukocytosis, hemorrhage or circulatory shock. During the last two decades, many studies have described DON toxicity using diverse animal species as a model. While the action of the toxin on peripheral organs and tissues is well documented, data illustrating its effect on the brain are significantly less abundant. Yet, DON is known to affect the central nervous system. Recent studies have provided new evidence and detail regarding the action of the toxin on the brain. The purpose of the present review is to summarize critical studies illustrating this central action of the toxin and to suggest research perspectives in this field.

show abstract

Body composition and hormonal effects following exposure to mycotoxin deoxynivalenol in the high‐fat diet‐induced obese mouse

Cited by 21 publications

References 35 publications

Peripubertal-onset but not adult-onset obesity increases IGF-I and drives development of lean mass, which may lessen the metabolic impairment in adult obesity

Peripubertal-onset but not adult-onset obesity increases IGF-I and drives development of lean mass, which may lessen the metabolic impairment in adult obesity

Assessment of T-2 toxin effect and its metabolite HT-2 toxin combined with insulin-like growth factor I, leptin and ghrelin on progesterone secretion by rabbit ovarian fragments

Advances in Deoxynivalenol Toxicity Mechanisms: The Brain as a Target

Contact Info

Product

Resources

About