Glyceroneogenesis Is Reduced and Glucose Uptake Is Increased in Adipose Tissue from Cafeteria Diet–Fed Rats Independently of Tissue Sympathetic Innervation

Chaves, Valéria Ernestânia; Frasson, Danúbia; Martins-Santos, M. E. S.; Boschini, Renata Polessi; Garófalo, Maria Antonieta Rissato; Festuccia, William; Kettelhut, Ísis C.; Migliorini, R H

doi:10.1093/jn/136.10.2475

Cited by 42 publications

(36 citation statements)

References 35 publications

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“…In addition, hypertension of CD-fed SHR increased further above controls, while the impaired insulin resistance also deteriorated further, as reflected by the slightly enhanced glucose and doubled insulin levels. Previous studies have demonstrated plasma glucose to be not or only marginally altered by various different high-calorie diets with insulin being usually doubled [27,33,45,47,49] . Thus, our findings on CD-fed SHR are within the range given in other reports.…”

Section: Discussionmentioning

confidence: 99%

Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome

et al. 2010

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Background/Aims: The metabolic syndrome (MS) has become an epidemiological problem in Western countries. We developed a diet-induced obese rat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic modifications. Methods: Spontaneously hypertensive rats (SHR) were allowed for 12 weeks to choose between a cafeteria diet (CD, 20.3 kJ/g) and standard rat chow (11.7 kJ/g). Controls received rat chow. Results: Body weight (BW) exceeded control levels when SHR were fed with CD. The increase in BW was attributed to enhanced energy intake. The abundance of abdominal fat as well as the plasma levels of leptin and triglycerides increased concomitant with glucose, insulin and C-peptide. This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. Conclusion: Increases in food intake and BW despite hyperleptinemia indicate leptin resistance following CD feeding. CD-fed SHR feature leptin and insulin resistance, hypertension and obesity, thus mimicking the situation of MS patients. As such, our model is more suitable than the genetically modified rat models used to study human MS.

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Section: Discussionmentioning

confidence: 99%

Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome

et al. 2010

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“…Because fasting causes an increase in pyruvate incorporation into G-3-P as well as an increase in PEPCK-C activity, glyceroneogenesis has been implicated in the enhanced TG-FA cycling associated with fasting. Furthermore, a diet high in carbohydrate decreases the activity of PEPCK-C in white adipose tissue (10); these changes are largely due to alterations in gene transcription (11). We hypothesized that after 48 h fast PEPCK-C activity would be increased, resulting in enhanced glyceroneogenesis in the adipose tissue, whereas a high carbohydrate, lipogenic diet would decrease PEPCK-C activity and lower flux over this pathway.…”

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confidence: 99%

Glyceroneogenesis Is the Dominant Pathway for Triglyceride Glycerol Synthesis in Vivo in the Rat

Nye

Hanson

Kalhan

2008

Journal of Biological Chemistry

155

177

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Triglyceride synthesis in mammalian tissues requires glycerol 3-phosphate as the source of triglyceride glycerol. In this study the relative contribution of glyceroneogenesis and glycolysis to triglyceride glycerol synthesis was quantified in vivo in adipose tissue, skeletal muscle, and liver of the rat in response to a chow diet (controls), 48-h fast, and lipogenic (high sucrose) diet. The rate of glyceroneogenesis was quantified using the tritium ([ 3 H 2 ]O) labeling of body water, and the contribution of glucose, via glycolysis, was determined using a [U-14 C]glucose tracer. In epididymal and mesenteric adipose tissue of control rats, glyceroneogenesis accounted for ϳ90% of triglyceride glycerol synthesis. Fasting for 48 h did not alter glyceroneogenesis in adipose tissue, whereas the contribution of glucose was negligible. In response to sucrose feeding, the synthesis of triglyceride glycerol via both glyceroneogenesis and glycolysis nearly doubled (versus controls); however, glyceroneogenesis remained quantitatively higher as compared with the contribution of glucose. Enhancement of triglyceride-fatty acid cycling by epinephrine infusion resulted in a higher rate of glyceroneogenesis in adipose tissue, as compared with controls, whereas the contribution of glucose via glycolysis was not measurable. Glyceroneogenesis provided the majority of triglyceride glycerol in the gastrocnemius and soleus. In the liver the fractional contribution of glyceroneogenesis remained constant (ϳ60%) under all conditions and was higher than that of glucose. Thus, glyceroneogenesis, in contrast to glucose, via glycolysis, is quantitatively the predominant source of triglyceride glycerol in adipose tissue, skeletal muscle, and liver of the rat during fasting and high sucrose feeding.Triglyceride synthesis is critical for the accretion of fat and for the transport of lipids in the blood. In addition, triglyceride synthesis is an essential component of the triglyceride-fatty acid (TG-FA) 3 cycle, in which fatty acids released from adipose tissue following lipolysis are re-esterified back to triglyceride (1, 2). Glycerol 3-phosphate (G-3-P) and fatty acyl-CoAs are the substrates for the synthesis of triglycerides. G-3-P can be formed by phosphorylation of glycerol via glycerol kinase or by the reduction of dihydroxyacetone phosphate via G-3-P dehydrogenase. Dihydroxyacetone phosphate can be derived from either glucose or pyruvate. Glycerol kinase, although highly active in the liver, is present at low activity in adipose tissue and skeletal muscle (3, 4). Glucose is generally considered to be the major carbon source for the synthesis of G-3-P in white and brown adipose tissue, skeletal muscle, and liver. However, the relative quantitative contribution of glucose and pyruvate (glyceroneogenesis) has not been examined systematically in vivo.Glyceroneogenesis, the de novo synthesis of G-3-P from precursors other than glucose and glycerol (i.e. pyruvate, lactate, alanine, and citric acid cycle anions) has long been suggested as a poten...

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“…CAF refers to free access to different foods of the human diet, palatable and high energetic, inducing obesity due to an excessive intake of energy . Earlier studies by our group showed that CAF induces body adiposity, nonalcoholic fatty liver disease and increases de novo fatty acid synthesis in the liver and in white and brown adipose tissues . CAF also increases serum insulin levels and activates the sympathetic flux to white and brown adipose tissue, but not to the liver …”

Section: Introductionmentioning

confidence: 82%

“…The use of this rapid and potent model for obesity induction may be useful in detecting new pathways for preventive or therapeutic interventions to treat human obesity . This diet delivers increased amounts of carbohydrates and leads to a buildup in body fat, white adipose tissue, and TAG …”

Section: Discussionmentioning

confidence: 99%

“…The CAF‐fed rats’ daily energy intake was around 40% greater (293 ± 13 vs 209 ± 4 kJ·100 g/bw −1 /d −1 ) than the control. In CAF‐fed rats, protein corresponded to 15% ± 1%, carbohydrate 65% ± 1%, and lipid 20% ± 1% of the total energy input, while control rats were fed 25%, 63%, and 12%, respectively . Body weight was consistently measured at fixed intervals.…”

Section: Methodsmentioning

confidence: 99%

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Evaluation of the effect of cafeteria diet on the kidney Na,K‐ATPase activity, and oxidative stress

Pinheiro

Melo

Sousa

et al. 2019

J of Cellular Biochemistry

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In this study, renal tissue, subdivided into the cortex and medulla of Wistar rats subjected to a cafeteria diet (CAF) for 24 days or to normal diet, was used to analyze whether the renal enzyme Na,K‐ATPase activity was modified by CAF diet, as well as to analyze the α1 subunit of renal Na,K‐ATPase expression levels. The lipid profile of the renal plasma membrane and oxidative stress were verified. In the Na,K‐ATPase activity evaluation, no alteration was found, but a significant decrease of 30% in the cortex was detected in the α1 subunit expression of the enzyme. There was a 24% decrease in phospholipids in the cortex of rats submitted to CAF, a 17% increase in cholesterol levels in the cortex, and a 23% decrease in the medulla. Lipid peroxidation was significantly increased in the groups submitted to CAF, both in the cortical region, 29%, and in the medulla, 35%. Also, a reduction of 45% in the glutathione levels was observed in the cortex and medulla with CAF. CAF showed a nearly two‐fold increase in glutathione peroxidase (GPX) activity in relation to the control group in the cortex and a 59% increase in the GPx activity in the medulla. In conclusion, although the diet was administered for a short period of time, important results were found, especially those related to the lipid profile and oxidative stress, which may directly affect renal function.

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Glyceroneogenesis Is Reduced and Glucose Uptake Is Increased in Adipose Tissue from Cafeteria Diet–Fed Rats Independently of Tissue Sympathetic Innervation

Cited by 42 publications

References 35 publications

Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome

Overfeeding-Induced Obesity in Spontaneously Hypertensive Rats: An Animal Model of the Human Metabolic Syndrome

Glyceroneogenesis Is the Dominant Pathway for Triglyceride Glycerol Synthesis in Vivo in the Rat

Evaluation of the effect of cafeteria diet on the kidney Na,K‐ATPase activity, and oxidative stress

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