Diet‐Induced Models of Obesity (DIO) in Rodents

Bagnol, Didier; Al-Shamma, Hussien; Behan, Dominic P.; Whelan, Kevin; Grottick, Andrew J.

doi:10.1002/0471142301.ns0938s59

Cited by 17 publications

(15 citation statements)

References 37 publications

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“…For these studies, we used diet to induce obesity because the United States obesity epidemic is driven primarily by consumption of calorically dense palatable foods, rather than by genetic mutations (14,15). Adult male rats fed a high-fat, palatable, nutritionally complete diet showed increased body weight over the 8-wk access period compared with controls fed standard rodent chow, with an effect of week (F 8,112 = 1,244.80, P < 0.0001) and diet group (F 1,14 = 32.34, P < 0.0001), and an interaction effect between week and diet group (F 8,112 = 33.84, P < 0.0001) (SI Appendix, Fig.…”

Section: Resultsmentioning

confidence: 99%

Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

Bocarsly

Fasolino

Kane

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

210

151

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Obesity is a major public health problem affecting overall physical and emotional well-being. Despite compelling data suggesting an association between obesity and cognitive dysfunction, this phenomenon has received relatively little attention. Neuroimaging studies in obese humans report reduced size of brain regions involved in cognition, but few studies have investigated the cellular processes underlying cognitive decline in obesity or the influence of obesity on cognition in the absence of obesity-related illnesses. Here, a rat model of diet-induced obesity was used to explore changes in brain regions important for cognition. Obese rats showed deficits on cognitive tasks requiring the prefrontal and perirhinal cortex. Cognitive deficits were accompanied by decreased dendritic spine density and synaptic marker expression in both brain regions. Microglial morphology was also changed in the prefrontal cortex. Detrimental changes in the prefrontal cortex and perirhinal cortex occurred before metabolic syndrome or diabetes, suggesting that these brain regions may be particularly vulnerable to early stage obesity.O besity is a growing public health concern, affecting more than one-third of the United States adult population (1). Obesity increases the incidence of diabetes, vascular disease, and mental illness, all of which reduce quality of life and place a heavy financial burden on patients and society. Less recognized consequences of obesity are its deleterious effects on cognitive function. Individual cognitive performance, both rudimentary and scholastic, declines with increases in body mass and energy consumption (2-5). These deficits can be observed throughout life, from childhood to late adulthood. Obesity is also associated with an increased incidence of mild cognitive impairment and dementia in the elderly (6).Some evidence suggests that obese individuals have decreased overall brain volume (7), with further studies indicating more specific reductions in the volume of brain regions important for cognition, including the hippocampus, prefrontal cortex (PFC), and anterior cingulate (5,8,9). Few studies, however, have investigated the cellular and biochemical mechanisms that might underlie obesityinduced changes in brain volume and cognitive function.Although clinical studies strongly suggest that obesity produces cognitive impairment and brain atrophy, it is difficult to determine whether these changes arise from obesity itself or from conditions often associated with obesity, like metabolic syndrome, diabetes, and vascular disease. Such conditions, even in the absence of obesity, have been linked to cognitive dysfunction and decreases in brain volume (10-13). Little research has been done exploring the effects of obesity on brain structure and cognition in obese, but otherwise healthy, individuals. To investigate whether obesity in the absence of obvious illness alters brain structure and function, we used a rat model of dietinduced obesity to assess the PFC, the perirhinal cortex (PRC), and the hippocampus...

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Section: Resultsmentioning

confidence: 99%

Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

Bocarsly

Fasolino

Kane

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

210

151

View full text Add to dashboard Cite

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“…Mice with high‐fat diet displayed extreme states of obesity‐based weighed gain (high fat vs. low fat: 32.22 ± 0.62 g vs. 23.1 ± 0.39 g, p < 0.01). The mean ratio of visceral fat to body weight was also significantly higher in HF compared to LF groups (5.32 ± 0.77% vs. 4.51 ± 0.75%) (Bagnol, Al‐Shamma, Behan, Whelan, & Grottick, ). Therefore, mice in the first and second groups were termed nonobese (LF) and obese (HF) respectively.…”

Section: Methodsmentioning

confidence: 99%

Effect of aerobic exercise, low‐fat and high‐fat diet on the testis tissue and sperm parameters in obese and nonobese mice model

et al. 2019

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Semen quality and male fertility depend on numerous factors such as age, environment, lifestyle, physical activity, genetic background and occupation. We aimed to access the effect of aerobic exercise, low‐ and high‐fat diet on mice testis tissue, and sperm function. Obese and nonobese male mice C57BL/6 were exposed to high fat (Hf) or low fat (Lf) and/or activity (Exe: exercise or Sed: sedentary). Finally, testicular morphometric characteristics, sperm concentration and motility (light microscopy), sperm morphology (eosin/nigrosin dye), lipid peroxidation (BODIPY C11 Probe), chromatin (acridine orange and chromomycin A3 staining) were compared within obese groups (Hf/Exe, Lf/Exe, Lf/Sed, Hf/Sed) and nonobese groups (Hf/Exe, Lf/Exe, Lf/Sed, Hf/Sed). Both exercise and diet interventions did not show any alteration in testicular morphological characteristics, sperm morphology and DNA fragmentation within both obese and nonobese groups (p > 0.05). Exercise and/or diet resulted in a significant increase in sperm concentration and motility within both groups (p < 0.05). Exercise in both groups leads to high percentage of lipid peroxidation (p < 0.05). Exercise intervention significantly improved sperm protamine deficiency within obese group (p < 0.05). We concluded that exercise intervention was more effective than diet in improvement of sperm function within obese groups.

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“…Diet-induced obesity (DIO) model simulates diet-related obesity of human the best among various obesity models and thus gets widely used in animal studies [10]. Its establishment depends on excessive intake of high-fat (HF) diet over time, generally for about 15 weeks [10].…”

Section: Introductionmentioning

confidence: 99%

Aberrant Periodontal and Systemic Immune Response of Overweight Rodents to Periodontal Infection

Takata

Zhao

Huang

et al. 2019

BioMed Research International

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This study aimed to explore periodontal and systemic immune response of overweight hosts to periodontitis. Forty C57 BL/6J male mice were divided into high (HF) or low fat (LF) diet groups and fed with the two diets, respectively, for 8 weeks. Each diet group was then divided into periodontitis (P) or control (C) groups (n = 10 per group) for 10-day ligation or sham-ligation. Overweight-related parameters including body weight were measured. Alveolar bone loss (ABL) was morphometrically analyzed and periodontal osteoclasts were stained. Periodontal immune response including leukocyte and macrophage number and inflammatory cytokines were analyzed by histology and quantitative PCR. Serum cytokine and lipid levels were quantified using electrochemiluminescence immunoassays, enzyme-linked immunosorbent assays, and biochemistry. It was found that HF group had 14.4% body weight gain compared with LF group (P < 0.01). ABL and periodontal osteoclast, leukocyte, and macrophage number were higher in P group than C group regardless of diet (P < 0.05). ABL and periodontal osteoclast number were not affected by diet regardless of ligation or sham-ligation. Leukocyte and macrophage number and protein level of tumor necrosis factor α (TNF-α) in periodontium and serum interleukin-6 level were downregulated by HF diet in periodontitis mice (P < 0.05). Periodontal protein level of TNF-α was highly correlated with serum interleukin-6 and low-density lipoprotein cholesterol levels (P < 0.01). These findings indicated that impaired immune response occurs both periodontally and systemically in preobesity overweight individuals. Given a well-reported exacerbating effect of obesity on periodontitis, overweight, if let uncontrolled, might place the individuals at potential risk for future periodontal tissue damage.

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Diet‐Induced Models of Obesity (DIO) in Rodents

Cited by 17 publications

References 37 publications

Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

Effect of aerobic exercise, low‐fat and high‐fat diet on the testis tissue and sperm parameters in obese and nonobese mice model

Aberrant Periodontal and Systemic Immune Response of Overweight Rodents to Periodontal Infection

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