Mice chronically fed a westernized experimental diet as a model of obesity, metabolic syndrome and osteoporosis

Demigné, Christian; Bloch-Faure, May; Picard, Nicolas; Sabboh, Houda; Besson, Catherine; Rémésy, Christian; Geoffroy, Valérie; Gaston, Anh-Thu; Nicoletti, Antonino; Hagège, Albert; Ménard, Joël; Meneton, Pierre

doi:10.1007/s00394-006-0599-6

Cited by 46 publications

(36 citation statements)

References 32 publications

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“…In the Western-type diet group, rats that gained the most body weight (Ͼ200 g, compared with ϳ150 -180 g in the nonresponder group) during the 9-wk observation period were designated as diet-induced obese rats and selected for further experiments (50% of initial number; n ϭ 20). These data are consistent with other studies showing that among outbred Sprague-Dawley rats or mice, approximately one-half develop diet-induced obesity (DIO) when kept on a Western-type diet (14,35).…”

Section: Experimental Designsupporting

confidence: 92%

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High-protein diet selectively reduces fat mass and improves glucose tolerance in Western-type diet-induced obese rats

Stengel

Goebel-Stengel

Wang

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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-Obesity is an increasing health problem. Because drug treatments are limited, diets remain popular. High-protein diets (HPD) reduce body weight (BW), although the mechanisms are unclear. We investigated physiological mechanisms altered by switching diet induced obesity (DIO) rats from Western-type diet (WTD) to HPD. Male rats were fed standard (SD) or WTD (45% calories from fat). After developing DIO (50% of rats), they were switched to SD (15% calories from protein) or HPD (52% calories from protein) for up to 4 weeks. Food intake (FI), BW, body composition, glucose tolerance, insulin sensitivity, and intestinal hormone plasma levels were monitored. Rats fed WTD showed an increased FI and had a 25% greater BW gain after 9 wk compared with SD (P Ͻ 0.05). Diet-induced obese rats switched from WTD to HPD reduced daily FI by 30% on day 1, which lasted to day 9 (Ϫ9%) and decreased BW during the 2-wk period compared with SD/SD (P Ͻ 0.05). During these 2 wk, WTD/HPD rats lost 72% more fat mass than WTD/SD (P Ͻ 0.05), whereas lean mass was unaltered. WTD/HPD rats had lower blood glucose than WTD/SD at 30 min postglucose gavage (P Ͻ 0.05). The increase of pancreatic polypeptide and peptide YY during the 2-h dark-phase feeding was higher in WTD/HPD compared with WTD/SD (P Ͻ 0.05). These data indicate that HPD reduces BW in WTD rats, which may be related to decreased FI and the selective reduction of fat mass accompanied by improved glucose tolerance, suggesting relevant benefits of HPD in the treatment of obesity. diet-induced obesity; food intake; high-protein diet; gut hormones OBESITY HAS BECOME EPIDEMIC, and by the year 2030, half of the adult population is predicted to be obese in the United States (54). Its prevalence is expanding worldwide in industrialized countries and spreading also to less developed countries; therefore "globesity" is taking over many parts of the world (see World Health Organization homepage). The plethora of health consequences related to obesity involves increased risk of developing adult-onset Type 2 diabetes mellitus, dyslipidemia, arteriosclerosis, and certain forms of cancer, including colorectal and pancreatic cancer (25). Therefore, obesity represents a major medical problem in the United States, and 12% of the entire health care costs are spent taking care of obesity-related comorbidities (52). A modest 5 to 10% body weight loss in obese subjects has been shown to result in improvements of these metabolic disturbances (21, 53).Although two antiobesity drugs have recently been approved, drug treatment options are still very limited (26), and therefore, dietary interventions remain popular. In particular, the use of a high-protein diet is considered a beneficial strategy to achieve a long-term reduction in body weight (8,22,47,48). However, the means by which an isocaloric high-protein diet reduces body weight are not well understood. There is some evidence that protein decreases appetite by increasing anorexigenic signaling (16,34,55) and stimulates thermogenesis (13,57,58) in experi...

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Section: Experimental Designsupporting

confidence: 92%

“…3A). During the remaining observation period (days [2][3][4][5][6][7][8][9][10][11][12][13][14], rats in the standard diet/standard diet group displayed an overall stable food intake with an average of 67.6 Ϯ 1.0 kcal/day (Fig. 3A).…”

Section: Western-type Diet Induces Obesitymentioning

confidence: 99%

High-protein diet selectively reduces fat mass and improves glucose tolerance in Western-type diet-induced obese rats

Stengel

Goebel-Stengel

Wang

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…have distinctive impacts on muscle insulin sensitivity (14,19), pancreatic insulin secretion (63,75), and induction of metabolic disturbances. High content of long-chain saturated fatty acids compared with their unsaturated counterparts [low unsaturation index (UI)] in the Western-type diet is considered to be a major cause of both the obesity and muscle insulin resistance (13,18). Although individual fatty acid composition of ceramides was studied in detail in animal models of T2D (50) and insulin-resistant human subjects (20), none of the studies addressed T1D models.…”

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confidence: 99%

Impact of insulin deprivation and treatment on sphingolipid distribution in different muscle subcellular compartments of streptozotocin-diabetic C57Bl/6 mice

Zabielski

Błachnio-Zabielska

Lanza

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Insulin deprivation in type 1 diabetes (T1D) individuals increases lipolysis and plasma free fatty acids (FFA) concentration, which can stimulate synthesis of intramyocellular bioactive lipids such as ceramides (Cer) and longchain fatty acid-CoAs (LCFa-CoAs). Ceramide was shown to decrease muscle insulin sensitivity, and at mitochondrial levels it stimulates reactive oxygen species production. Here, we show that insulin deprivation in streptozotocin diabetic C57BL/6 mice increases quadriceps muscle Cer content, which was correlated with a concomitant decrease in the body fat and increased plasma FFA, glycosylated hemoglobin level (%Hb A 1c), and muscular LCFa-CoA content. The alternations were accompanied by an increase in protein expression in LCFa-CoA and Cer synthesis (FATP1/ACSVL5, CerS1, CerS5), a decrease in the expression of genes implicated in muscle insulin sensitivity (GLUT4, GYS1), and inhibition of insulin signaling cascade by Akt␣ and GYS3␤ phosphorylation under acute insulin stimulation. Both the content and composition of sarcoplasmic fraction sphingolipids were most affected by insulin deprivation, whereas mitochondrial fraction sphingolipids remained stable. The observed effects of insulin deprivation were reversed, except for content and composition of LCFa-CoA, CerS protein expression, GYS1 gene expression, and phosphorylation status of Akt and GYS3␤ when exogenous insulin was provided by subcutaneous insulin implants. Principal component analysis and Pearson's correlation analysis revealed close relationships between the features of the diabetic phenotype, the content of LCFa-CoAs and Cers containing C18-fatty acids in sarcoplasm, but not in mitochondria. Insulin replacement did not completely rescue the phenotype, especially regarding the content of LCFa-CoA, or proteins implicated in Cer synthesis and muscle insulin sensitivity. These persistent changes might contribute to muscle insulin resistance observed in T1D individuals. type 1 diabetes; skeletal muscle; mitochondria; ceramide; long-chain fatty acid-coenzyme A METICULOUS GLYCEMIC CONTROL in type 1 diabetic (T1D) individuals can be achieved by administration of prandial, shortacting, and long-acting insulin to mimic ␤-cell secretion in response to varying nutrient levels. Metabolic control in these individuals and stringent adherence to guidelines normalize the plasma glucose and glycosylated hemoglobin levels (%Hb A 1c ) and allow for relatively normal life in T1D. Yet T1D individuals are at greater risk of developing cardiovascular disorders and also known to develop insulin resistance (12, 17). The molecular mechanisms responsible for insulin resistance in T1D subjects are unclear, but variable glucose concentrations (28, 70), advanced glycation end products (62, 73), or desensitization of target tissues by insulin (61) have been proposed. Subcutaneous insulin delivery using an insulin pump partially mimics ␤-cell insulin secretion. However, unlike in nondiabetic individuals with twofold higher hepatic insulin concentration than in ...

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“…Diet is considered the most frequent cause of obesity in industrialized and urbanized countries [18]. In the present study, it was possible to verify the effectiveness of the cafeteria diet to induce obesity.…”

Section: Discussionmentioning

confidence: 84%

Evaluation of Bone Tissue After Cafeteria-Diet-Induced Obesity and Periodontitis in Rats

Nascimento¹,

Felipetti²,

Cassol³

et al. 2015

J Endocrinol Metab

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Mice chronically fed a westernized experimental diet as a model of obesity, metabolic syndrome and osteoporosis

Abstract: These data suggest that a model of westernized diet could be appropriate for exploring the effects of mutations, drugs, or specific nutritional factors in animals and could be more relevant for human situations.

Cited by 46 publications

References 32 publications

High-protein diet selectively reduces fat mass and improves glucose tolerance in Western-type diet-induced obese rats

High-protein diet selectively reduces fat mass and improves glucose tolerance in Western-type diet-induced obese rats

Impact of insulin deprivation and treatment on sphingolipid distribution in different muscle subcellular compartments of streptozotocin-diabetic C57Bl/6 mice

Evaluation of Bone Tissue After Cafeteria-Diet-Induced Obesity and Periodontitis in Rats

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