Diet-induced models for obesity and type 2 diabetes

Reuter, T

doi:10.1016/j.ddmod.2007.09.004

Cited by 49 publications

(50 citation statements)

References 35 publications

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“…In agreement with human obesity 23 and rat models of diet-induced obesity, 21,24,25 high-fat feeding was associated with hypertension and hyperleptinemia. In contrast to the human phenotype, blood glucose levels were unaltered in obesity; however, overt hyperglycaemia has rarely been reported in studies using Sprague-Dawley rats 26 and in agreement with our data, insulin resistance is common and its severity seems to be dependent on the fat content of the diet and duration of feeding. 27 The initial caloric restriction to 40 kcal/d was chosen to mimic human dieting 28 and successfully produced a significant reduction in body weight during the 4-week period, consistent with that observed in other rodent models.…”

Section: Discussionsupporting

confidence: 81%

Obesity-Related Perivascular Adipose Tissue Damage Is Reversed by Sustained Weight Loss in the Rat

Bussey

Withers

Aldous

et al. 2016

ATVB

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Objective-Perivascular adipose tissue (PVAT) exerts an anticontractile effect in response to various vasoconstrictor agonists, and this is lost in obesity. A recent study reported that bariatric surgery reverses the damaging effects of obesity on PVAT function. However, PVAT function has not been characterized after weight loss induced by caloric restriction, which is often the first line treatment for obesity. Approach and Results-Contractility studies were performed using wire myography on small mesenteric arteries with and without PVAT from control, diet-induced obese, calorie restricted and sustained weight loss rats. Changes in the PVAT environment were assessed using immunohistochemistry. PVAT from healthy animals elicited an anticontractile effect in response to norepinephrine. This was abolished in diet-induced obesity through a mechanism involving increased local tumor necrosis factor-α and reduced nitric oxide bioavailability within PVAT. Sustained weight loss led to improvement in PVAT function associated with restoration of adipocyte size, reduced tumor necrosis factor-α, and increased nitric oxide synthase function. This was associated with reversal of obesity-induced hypertension and normalization of plasma adipokine levels, including leptin and insulin. Conclusions-We have shown that diet-induced weight loss reverses obesity-induced PVAT damage through a mechanism involving reduced inflammation and increased nitric oxide synthase activity within PVAT. These data reveal inflammation and nitric oxide synthase, particularly endothelial nitric oxide synthase, as potential targets for the treatment of PVAT dysfunction associated with obesity and metabolic syndrome.

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Section: Discussionsupporting

confidence: 81%

Obesity-Related Perivascular Adipose Tissue Damage Is Reversed by Sustained Weight Loss in the Rat

Bussey

Withers

Aldous

et al. 2016

ATVB

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“…Besides, female animal models are better responders to high-fat feeding, mimicking susceptibility to obesity in humans. However, in a recent review, male mice and rats are introduced as 'gold standards' for studying dietary obesity (7) . This might be because of the oestrous cycle of the female animals which is repeated every 4 -6 d and can affect the food intake of the animal during this period (301) .…”

Section: Sex Differencesmentioning

confidence: 99%

“…Rats and mice known as the standard models for studying dietary obesity are different in their susceptibility to obesity: outbred Sprague-Dawley rats, Wistar rats and C57BL/6C mice can be easily categorised to prone and resistant phenotypes with ad libitum access to high-fat diets (7,8,21) . There are also strains known as genetically obese, such as Zucker fa/fa rats and ob/ob mice (8,35) .…”

Section: Susceptibility To Obesitymentioning

confidence: 99%

“…Its prevalence is increasing, with 400 million obese and 1·6 billion overweight adults around the world (1) . Although genetics plays a role in the regulation of body weight, body size and body composition and the metabolic response to feeding in humans (2 -6) and in animals (7,8) , the increase in worldwide obesity in a short period of time cannot be explained by genetics; there are individual differences in genetic susceptibility to environmental factors such as diet (2,6,9 -11) .…”

Section: Introductionmentioning

confidence: 99%

“…Since under-reporting is an important bias in epidemiological studies on diet and obesity in human subjects (32 -34) , animal models have been widely utilised for experiments on dietary obesity (7,8,35,36) . Usually high-fat diets within the range of 30-78 % of total energy intake are used (21) either by adding a particular fat to the animal's diet or using an assortment of fat-and sugar-rich supermarket foods (cafeteria diet) -for studying obesity in rats (24,37 -46) and mice (25,47 -52) .…”

Section: Introductionmentioning

confidence: 99%

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High-fat diet-induced obesity in animal models

2010

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Epidemiological studies have shown a positive relationship between dietary fat intake and obesity. Since rats and mice show a similar relationship, they are considered an appropriate model for studying dietary obesity. The present paper describes the history of using high-fat diets to induce obesity in animals, aims to clarify the consequences of changing the amount and type of dietary fats on weight gain, body composition and adipose tissue cellularity, and explores the contribution of genetics and sex, as well as the biochemical basis and the roles of hormones such as leptin, insulin and ghrelin in animal models of dietary obesity. The major factors that contribute to dietary obesity -hyperphagia, energy density and post-ingestive effects of the dietary fat -are discussed. Other factors that affect dietary obesity including feeding rhythmicity, social factors and stress are highlighted. Finally, we comment on the reversibility of high-fat diet-induced obesity.

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Systemically impaired fracture healing in small animal research: A review of fracture repair models

Ryan

Magony

Gortler

et al. 2021

Journal Orthopaedic Research

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Fracture healing is a complex process requiring mechanical stability, an osteoconductive matrix, and osteoinductive and osteogenic biology. This intricate process is easily disrupted by various patient factors such as chronic disease and lifestyle. As the medical complexity and age of patients with fractures continue to increase, the importance of developing relevant experimental models is becoming paramount in preclinical research. The objective of this review is to describe the most common small animal models of systemically impaired fracture healing used in the orthopedic literature including osteoporosis, diabetes mellitus, smoking, alcohol use, obesity, and ageing. This review will provide orthopedic researchers with a summary of current models of systemically impaired fracture healing used in small animals and present an overview of the methods of induction for each condition.

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Diet-induced models for obesity and type 2 diabetes

Cited by 49 publications

References 35 publications

Obesity-Related Perivascular Adipose Tissue Damage Is Reversed by Sustained Weight Loss in the Rat

Obesity-Related Perivascular Adipose Tissue Damage Is Reversed by Sustained Weight Loss in the Rat

High-fat diet-induced obesity in animal models

Systemically impaired fracture healing in small animal research: A review of fracture repair models

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