Time-Restricted Feeding Improves Body Weight Gain, Lipid Profiles, and Atherogenic Indices in Cafeteria-Diet-Fed Rats: Role of Browning of Inguinal White Adipose Tissue

Time-restricted feeding (TRF) showed a potent effect in preventing obesity and improving metabolicoutcomes in several animal models of obesity. However, there is, as of yet, scarce evidence concerning its effectiveness against obesogenic challenges that more accurately mimic human Western diets, such as the cafeteria diet. Moreover, the mechanism for its efficacy is poorly understood. White adipose browning has been linked to body weight loss. Herein, we tested whether TRF has the potential to induce browning of inguinal white adipose tissue (iWAT) and to attenuate obesity and associated dyslipidemia in a cafeteria-diet-induced obesity model. Male Wistar rats were fed normal laboratory chow (NC) or cafeteria diet (CAF) for 16 weeks and were subdivided into two groups that were subjected to either ad libitum (ad lib, A) or TRF (R) for 8 h per day. Rats under the TRF regimen had a lower body weight gain and adiposity than the diet-matchedad lib rats, despite equivalent levels of food intake and locomotor activity. In addition, TRF improved the deranged lipid profile (total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL-c), low-density lipoprotein (LDL-c)) and atherogenic indices (atherogenic index of plasma (AIP), atherogenic coefficient (AC), coronary risk index (CRI) in CAF-fed rats. Remarkably, TRF resulted in decreased size of adipocytes and induced emergence of multilocular brown-like adipocytes in iWAT of NC- and CAF-fed rats. Protein expression of browning markers, such as uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), were also up-regulated in the iWAToftime-restricted NC- or CAF-fed rats. These findings suggest that a TRF regimen is an effective strategy to improve CAF diet-induced obesity, probably via a mechanismthe involving WAT browning process.

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Time-Restricted Feeding Improves Body Weight Gain, Lipid Profile, and Atherogenic Indices in Cafeteria Diet-fed Rats: Role of Browning Inguinal White Adipose Tissue

10.20944/preprints202006.0134.v1 ◽

2020 ◽

Author(s):

Samira Aouichat ◽

Souhila Bouguerra-Aouichat ◽

Ahmad Agil

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Lipid Profile ◽

White Adipose Tissue ◽

Body Weight Gain ◽

Density Lipoprotein ◽

Cafeteria Diet ◽

Restricted Feeding ◽

Atherogenic Indices

Time-restricted feeding (TRF) showed a potent effect in preventing obesity and improving metabolic outcomes in several animal model of obesity; however, there is, as yet, scarce evidence about its effectiveness against obesogenic challenge that more accurately mimic the human Western diets, such as cafeteria diet. Moreover, the mechanism for its efficacy is poorly understood. White adipose browning has been linked to body weight loss. Herein, we tested whether TRF has the potential to induce browning of inguinal white adipose tissue (iWAT) and to attenuate obesity and associated dyslipidemia in cafeteria diet-induced obesity model. Male Wistar rats, fed normal laboratory chow (NC) or cafeteria diet (CAF) for 16 weeks, were subdivided into two groups that were subjected to either ad libitum (ad lib, A) or TRF (R) for 8 hours per day. Rats under TRF regimen had a lower body weight gain and adiposity compared with their diet-matched ad lib rats, despite equivalent levels of food intake and locomotor activity. In addition, TRF improved the deranged lipid profile [total cholesterol (TC); triglycerides (TG); high density lipoprotein (HDL-c); low density lipoprotein (LDL-c)] and atherogenic indices [atherogenic index of plasma (AIP); atherogenic coefficient (AC); coronary risk index (CRI)] in rats fed CAF diet. Remarkably, TRF resulted in decreased size of adipocytes and induced emergence of multilocular brown-like adipocytes in iWAT of NC- and CAF-fed rats. Protein expression of browning markers, such as uncoupling protein-1 (UCP1) and peroxisome proliferator activated receptor gamma coactivator 1-alpha (PGC1α) in iWAT were also up-regulated in time restricted NC- or CAF-fed rats. These findings suggest that TRF regimen is an effective strategy to improve obesity and associated dyslipidemia induced by CAF-diet, probably via a mechanism involving WAT browning process.

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Front Cover: Nicotinamide Protects Against Diet‐Induced Body Weight Gain, Increases Energy Expenditure, and Induces White Adipose Tissue Beiging

Molecular Nutrition & Food Research ◽

10.1002/mnfr.202170027 ◽

2021 ◽

Vol 65 (11) ◽

pp. 2170027

Author(s):

Karen Alejandra Méndez‐Lara ◽

Elisabeth Rodríguez‐Millán ◽

David Sebastián ◽

Rosi Blanco‐Soto ◽

Mercedes Camacho ◽

...

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Energy Expenditure ◽

White Adipose Tissue ◽

Body Weight Gain ◽

Front Cover

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Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00358.2017 ◽

2018 ◽

Vol 315 (1) ◽

pp. E29-E37 ◽

Cited By ~ 3

Author(s):

Mariana Peduti Halah ◽

Paula Beatriz Marangon ◽

Jose Antunes-Rodrigues ◽

Lucila L. K. Elias

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Food Intake ◽

White Adipose Tissue ◽

Energy Homeostasis ◽

Body Weight Gain ◽

Adult Life ◽

Male Rats ◽

Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

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Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α

British Journal Of Nutrition ◽

10.1017/s0007114507207627 ◽

2007 ◽

Vol 97 (2) ◽

pp. 389-398 ◽

Cited By ~ 131

Author(s):

Patricia Pérez-Matute ◽

Nerea Pérez-Echarri ◽

J. Alfredo Martínez ◽

Amelia Marti ◽

María J. Moreno-Aliaga

Keyword(s):

Gene Expression ◽

Insulin Resistance ◽

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Body Weight Gain ◽

Control Diet ◽

Cafeteria Diet ◽

High Fat ◽

Beneficial Effects

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

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Individual housing of male C57BL/6J mice after weaning impairs growth and predisposes for obesity

10.1101/834416 ◽

2019 ◽

Author(s):

Lidewij Schipper ◽

Steffen van Heijningen ◽

Giorgio Karapetsas ◽

Eline M. van der Beek ◽

Gertjan van Dijk

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Energy Intake ◽

White Adipose Tissue ◽

Body Weight Gain ◽

Tissue Mass ◽

Individual Housing ◽

Adipose Tissue Mass ◽

Obesogenic Diet

AbstractIndividual housing from weaning onwards resulted in reduced growth rate during adolescence in male C57Bl/6J mice that were housed individually, while energy intake and energy expenditure were increased compared to socially housed counterparts. At 6 weeks of age, these mice had reduced lean body mass, but significantly higher white adipose tissue mass compared to socially housed mice. Body weight gain of individually housed animals exceeded that of socially housed mice during adulthood, with elevations in both energy intake and expenditure. At 18 weeks of age, individually housed mice showed higher adiposity and higher mRNA expression of UCP-1 in inguinal white adipose tissue. Exposure to an obesogenic diet starting at 6 weeks of age further amplified body weight gain and adipose tissue deposition. This study shows that post-weaning individual housing of male mice results in impaired adolescent growth and higher susceptibility to obesity in adulthood. Mice are widely used to study obesity and cardiometabolic comorbidities. For (metabolic) research models using mice, (social) housing practices should be carefully considered and regarded as a potential confounder due to their modulating effect on metabolic health outcomes.

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Nicotinamide Protects Against Diet‐Induced Body Weight Gain, Increases Energy Expenditure and Induces White Adipose Tissue Beiging

Molecular Nutrition & Food Research ◽

10.1002/mnfr.202100111 ◽

2021 ◽

pp. 2100111

Author(s):

Karen Alejandra Méndez‐Lara ◽

Elisabeth Rodríguez‐Millán ◽

David Sebastián ◽

Rosi Blanco‐Soto ◽

Mercedes Camacho ◽

...

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Energy Expenditure ◽

White Adipose Tissue ◽

Body Weight Gain

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Abstract 295: Microsomal Prostaglandin E Synthase 1 Deficiency Attenuates Diet-Induced Obesity and Promotes the Formation of Brite Adipose Tissue

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.32.suppl_1.a295 ◽

2012 ◽

Vol 32 (suppl_1) ◽

Author(s):

Natalie J Moretz ◽

Nicholas Hatch ◽

Sarah Srodulski ◽

Victoria L King

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Marked Reduction ◽

Body Weight Gain ◽

Prostaglandin E ◽

Low Grade ◽

Prostaglandin E Synthase ◽

Diet Induced Obesity ◽

Microsomal Prostaglandin E Synthase

Mice deficient in adipocyte specific phospholipases A2 have a marked reduction in prostaglandin E2 (PGE2) levels and are resistant to the development of diet-induced obesity. Clinical data suggest that obesity is a chronic low grade inflammatory disease, characterized by the influx of inflammatory cells into the adipose tissue. During a chronic inflammatory state, microsomal prostaglandin E synthase-1 (mPGES-1) is the primary source of PGE2. We have previously demonstrated that mice deficient in mPGES-1 (KO) have a marked reduction in body weight gain and adiposity compared to littermate controls (WT) fed a high fat (HF) diet with a concomitant reduction in urinary PGE2 concentrations and an increase in urinary PGI2 concentrations. The reduction in weight gain is not for accounted by alterations in food intake or locomotor activity. However, resting metabolic rate, measured by indirect calorimetry, was increased in KO mice compared to WT fed a HF diet. Moreover, body temperature was also increased in KO mice compared to WT mice (37.0 ± 0.2 vs 35.8 ± 0.2; P < 0.05) fed a HF diet. Taken together these data suggest that mPGES-1 deficiency increases energy expenditure in response to feeding a HF diet. Analysis of white adipose tissue (WAT) depots demonstrated an increase in number of smaller adipocytes per unit area in the KO mice compared to WT mice. The WAT from KO mice also had a marked decrease in triglyceride content, F4/80 staining and CD86 staining with a concomitant increase in CD206 staining suggesting an attenuation in macrophage recruitment into the WAT as well as an M2 phenotype. Additionally, COX-2 and UCP-1 and PPAR-γ expression were increased in WAT depots with a concomitant localization of multi-locular adipocytes in WAT depots, demonstrating the presence of brown adipocytes in WAT depots in KO mice fed a HF diet. These data suggest that the reduction in body weight gain in the KO mice may be due an increase in thermogenesis mediated by the formation of brite adipose tissue in WAT depots.

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Supplementation with Lactiplantibacillus Plantarum IMC 510 Modifies Microbiota Composition and Prevents Body Weight Gain Induced by Cafeteria Diet in Rats

International Journal of Molecular Sciences ◽

10.3390/ijms222011171 ◽

2021 ◽

Vol 22 (20) ◽

pp. 11171

Author(s):

Maria Vittoria Micioni Di Bonaventura ◽

Maria Magdalena Coman ◽

Daniele Tomassoni ◽

Emanuela Micioni Di Bonaventura ◽

Luca Botticelli ◽

...

Keyword(s):

Body Weight ◽

Weight Gain ◽

Body Weight Gain ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Probiotic Strain ◽

Hepatic Lipid Accumulation ◽

Beneficial Effects ◽

Diet Induced Obesity ◽

The Impact

Changes in functionality and composition of gut microbiota (GM) have been associated and may contribute to the development and maintenance of obesity and related diseases. The aim of our study was to investigate for the first time the impact of Lactiplantibacillus (L.) plantarum IMC 510 in a rat model of diet-induced obesity, specifically in the cafeteria (CAF) diet. This diet provides a strong motivation to voluntary overeat, due to the palatability and variety of selected energy-dense foods. The oral administration for 84 days of this probiotic strain, added to the CAF diet, decreased food intake and body weight gain. Accordingly, it ameliorated body mass index, liver and white adipose tissue weight, hepatic lipid accumulation, adipocyte size, serum parameters, including glycemia and low-density lipoprotein levels, in CAF fed rats, potentially through leptin control. In this scenario, L. plantarum IMC 510 showed also beneficial effects on GM, limiting the microbial imbalance established by long exposure to CAF diet and preserving the proportion of different bacterial taxa. Further research is necessary to better elucidate the relationship between GM and overweight and then the mechanism of action by which L. plantarum IMC 510 modifies weight. However, these promising results prompt a clear advantage of probiotic supplementation and identify a new potential probiotic as a novel and safe therapeutic approach in obesity prevention and management.

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Small-Molecule Insulin Mimetic Reduces Hyperglycemia and Obesity in a Nongenetic Mouse Model of Type 2 Diabetes

Endocrinology ◽

10.1210/en.2004-0610 ◽

2004 ◽

Vol 145 (11) ◽

pp. 5259-5268 ◽

Cited By ~ 16

Author(s):

Mathias Z. Strowski ◽

Zhihua Li ◽

Deborah Szalkowski ◽

Xiaolan Shen ◽

Xiao-Ming Guan ◽

...

Keyword(s):

Type 2 Diabetes ◽

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Mouse Model ◽

Small Molecule ◽

White Adipose Tissue ◽

Body Weight Gain ◽

Nonesterified Fatty Acids

Abstract Adiposity positively correlates with insulin resistance and is a major risk factor of type 2 diabetes. Administration of exogenous insulin, which acts as an anabolic factor, facilitates adipogenesis. Recently nonpeptidal insulin receptor (IR) activators have been discovered. Here we evaluate the effects of the orally bioavailable small-molecule IR activator (Compound-2) on metabolic abnormalities associated with type 2 diabetes using a nongenetic mouse model in comparison with the effects of a novel non-thiazolidinedione (nTZD) peroxisome proliferator-activated receptor-γ agonist. Both Compound-2 and nTZD alleviated fasting and postprandial hyperglycemia; accelerated glucose clearance rate; and normalized plasma levels of nonesterified fatty acids, triglycerides, and leptin. Unlike nTZD, which increased body weight gain, and total fat mass, which is a common feature for PPARγ agonists, Compound-2 prevented body weight gain and hypertrophy of brown, and white adipose tissue depots and the development of hepatic steatosis in the mouse model of type 2 diabetes. The effect of the two compounds on proximal steps in insulin signal transduction pathway was analyzed in tissues. Compound-2 enhanced insulin-stimulated phosphorylation of IR tyrosine and/or Akt in the liver, skeletal muscle, and white adipose tissue, whereas nTZD potentiated the phosphorylation of IR and Akt in the adipose tissue only. In conclusion, small-molecule IR activators have unique features as insulin sensitizers and hold potential utility in the treatment of type 2 diabetes and obesity.

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Effect of Honey & Olive Oil Supplemented Bio-Yoghurt Feeding on Lipid Profile, Blood Glucose and Hematological Parameters in Rats

Current Nutrition & Food Science ◽

10.2174/1573401313666170905160124 ◽

2019 ◽

Vol 15 (2) ◽

pp. 140-147

Author(s):

Magdy M. Ismail ◽

El-Tahra M. Ammar ◽

Abd El-Wahab E. Khalil ◽

Mohamed Z. Eid

Keyword(s):

Body Weight ◽

Weight Gain ◽

Blood Glucose ◽

Olive Oil ◽

Body Weight Gain ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Lipoprotein Cholesterol ◽

Low Density ◽

Low Density Lipoprotein Cholesterol

Background and Objective: Yoghurt, especially bio-yoghurt has long been recognized as a product with many health benefits for consumers. Also, honey and olive oil have considerable nutritional and health effects. So, the effect of administration of yoghurt made using ABT culture and fortified with honey (2 and 6%), olive oil (1 and 4%) or honey + olive oil (2+1 and 6+4% respectively) on some biological and hematological properties of rats was investigated.Methods:The body weight gain, serum lipid level, blood glucose level, serum creatinine level, Glutamic Oxaloacetic Transaminase (GOT) activity, Glutamic Pyruvic Transaminase (GPT) activity, leukocytes and lymphocytes counts of rats were evaluated.Results:Blending of bio-yoghurt with rats' diet improved body weight gain. Concentrations of Total plasma Cholesterol (TC), High-Density Lipoprotein cholesterol (HDL), Low-Density Lipoprotein cholesterol (LDL), Very Low-Density Lipoprotein cholesterol (VLDL) and Triglycerides (TG) significantly lowered in plasma of rats fed bio-yoghurt. Levels of TC, LDL, VLDL, and TG also decreased in rat groups feed bio-yoghurt supplemented with honey and olive oil. LDL concentrations were reduced by 10.32, 18.51, 34.17, 22.48, 43.30% in plasma of rats fed classic starter yoghurt, ABT yoghurt, ABT yoghurt contained 6% honey, ABT yoghurt contained 4% olive oil and ABT yoghurt contained 6% honey + 4% olive oil respectively. The blood glucose, serum creatinine, GOT and GPT values of rats decreased while white blood cells and lymphocytes counts increased by feeding bioyoghurt contained honey and olive oil.Conclusion:The findings enhanced the multiple therapeutic effects of bio-yoghurt supplemented with honey and olive oil.

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