Obesity, insulin resistance and diabetes in the sand rat exposed to a hypercaloric diet; possible protective effect for IL1-β

Khalkhal, Ali; Haddar, Aomar; Semiane, N.; Mallek, A.; Abdelmalek, Abdelouadoud; Castex, Françoise; Gross, René; Dahmani, Y.

doi:10.1016/j.crvi.2012.03.003

Cited by 13 publications

(7 citation statements)

References 47 publications

(41 reference statements)

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“…SO was considered as a control group (C-SO), mainly because it contains adequate levels of PUFA, n − 6/n − 3 ratio within acceptable limits [38][39][40], and by its elevated consumption worldwide [25,37]. The two experimental groups (C-SO and HVF) were isocaloric in order to prevent metabolic differences between animals of different experimental groups [41,42] from interfering with the antioxidant defense system [43] and dopamine and serotonin neurotransmission [44]. The consumption of the diets was monitored every other day.…”

Section: Methodsmentioning

confidence: 99%

Chronic consumption of trans fat can facilitate the development of hyperactive behavior in rats

Pase

Trevizol

Kuhn

et al. 2015

Physiology & Behavior

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Section: Methodsmentioning

confidence: 99%

Chronic consumption of trans fat can facilitate the development of hyperactive behavior in rats

Pase

Trevizol

Kuhn

et al. 2015

Physiology & Behavior

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“…The occurrence of spontaneously obesity in the Meriones unguiculatus species of gerbils was reported several decades ago, when researchers observed that 10% of the animals became obese and showed metabolic alterations, even when fed standard diet (Vincent, Rodrick & Sodeman jr, 1979). Other species of desert rats, or gerbils, may also develop obesity when their typical diet is changed to standard rodent chow, such as Psammomys obesus (Khalkhal et al, 2012). Some studies addressed metabolic and immunological disorders related to obesity in this model of naturally obese animals (Xu, Liu & Wang, 2011; Liu, Xu & Wang, 2012).…”

Section: Introductionmentioning

confidence: 99%

Obesity-induced diet leads to weight gain, systemic metabolic alterations, adipose tissue inflammation, hepatic steatosis, and oxidative stress in gerbils (Meriones unguiculatus)

Ventura

Fortes

Santiago

et al. 2017

PeerJ

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BackgroundNowadays, the number of obese people in the world has reached alarming proportions. During the expansion of adipose tissue, a number of functions such as activation and release of cytokines and hormones may be affected. This leads the body to a pro-inflammatory pattern, which may affect the proper functioning of many tissues. Thus, studying the mechanisms by which obesity induces physiological disorders is necessary, and may be facilitated by the use of animal models, in particular rodents. We sought to characterize the metabolic and adipose tissue changes resulting from a diet rich in fats and simple sugars in gerbils.MethodsWe divided 14 gerbils into two experimental groups that received a diet rich in simple carbohydrates and fats with 5,86 kcal/g (OB, n = 7) or a standard diet with 4.15 kcal/g (CT; n = 7) for 11 weeks. The animals had free access to water and food. The animal weight and food consumption were measured weekly. Blood, adipose tissue and liver of each animal were collected at the end of experiment. The following parameters were determined: cholesterol (COL), triglycerides (TGL) and glycemia (GLI) in the plasma; cytokines (IL-6, IL-10 and TNF-α) and hormones (adiponectin and leptin) in adipose tissue; activity of superoxide dismutase (SOD) and catalase (CAT), extraction and differentiation of fat and histology in liver.ResultsThe consumption of a diet rich in simple carbohydrates and fats led to increased total body weight and increased relative weights of liver and adipose tissue. In addition, we observed increased fasting glucose levels and circulating triglycerides, along with high TNF-α production in adipose tissue and increased total fat, cholesterol and triglyceride contents in the liver, contributing to higher intensity of hepatic steatosis. On the other hand, the animals of this group showed depletion in the enzyme activity of SOD and CAT in the liver, as well as reduction of IL-10 and adiponectin levels in adipose tissue.DiscussionHigh intake of saturated fat and simple carbohydrates establish the gerbil as an experimental model for the study of metabolic and hepatic abnormalities resulting from obesity.

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“…IL-1 modulates glucose homeostasis by impairing insulin signaling, modulating insulin secretion, augmenting insulinindependent glucose uptake, increasing energy expenditure, and stimulating autonomic nervous system activity (58,70,97,107). Depending on the dose, IL-1 can induce hypoglycemia or hyperglycemia (70,138).…”

Section: Inflammation: Impact On Energy Expenditure and Glucose Homeomentioning

confidence: 99%

Inflammation during obesity is not all bad: evidence from animal and human studies

McGuinness

2013

American Journal of Physiology-Endocrinology and Metabolism

137

119

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Chronic inflammation is a characteristic of obesity and is associated with accompanying insulin resistance, a hallmark of type 2 diabetes mellitus (T2DM). Although proinflammatory cytokines are known for their detrimental effects on adipose tissue function and insulin sensitivity, their beneficial effects in the regulation of metabolism have not drawn sufficient attention. In obesity, inflammation is initiated by a local hypoxia to augment angiogenesis and improve adipose tissue blood supply. A growing body of evidence suggests that macrophages and proinflammatory cytokines are essential for adipose remodeling and adipocyte differentiation. Phenotypes of multiple lines of transgenic mice consistently suggest that proinflammatory cytokines increase energy expenditure and act to prevent obesity. Removal of proinflammatory cytokines by gene knockout decreases energy expenditure and induces adult-onset obesity. In contrast, elevation of proinflammatory cytokines augments energy expenditure and decreases the risk for obesity. Anti-inflammatory therapies have been tested in more than a dozen clinical trials to improve insulin sensitivity and glucose homeostasis in patients with T2DM, and the results are not encouraging. One possible explanation is that anti-inflammatory therapies also attenuate the beneficial effects of inflammation in stimulating energy expenditure, which may have limited the efficacy of the treatment by promoting energy accumulation. Thus, the positive effects of proinflammatory events should be considered in evaluating the impact of inflammation in obesity and type 2 diabetes.

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Obesity, insulin resistance and diabetes in the sand rat exposed to a hypercaloric diet; possible protective effect for IL1-β

Cited by 13 publications

References 47 publications

Chronic consumption of trans fat can facilitate the development of hyperactive behavior in rats

Chronic consumption of trans fat can facilitate the development of hyperactive behavior in rats

Obesity-induced diet leads to weight gain, systemic metabolic alterations, adipose tissue inflammation, hepatic steatosis, and oxidative stress in gerbils (Meriones unguiculatus)

Inflammation during obesity is not all bad: evidence from animal and human studies

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