Effects of pyruvate and dihydroxyacetone consumption on the growth and metabolic state of obese Zucker rats

Cortez, M. Y.; Torgan, C. E.; Brozinick, Joseph T.; Miller, Robert H.; Ivy, John L.

doi:10.1093/ajcn/53.4.847

Cited by 37 publications

(15 citation statements)

References 15 publications

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“…throughout the duration of the trial Johnstone et al (1989) found that supplementation of pyruvate/dihydroxyacetone (1 : 1; Pyr/D) to the diet significantly decreased the BW of Single Comb White Leghorn pullets. Cortez et al (1991), and Ivy et al (1994) also showed that Pyr fed for 3 to 5 weeks to rats results in decreased BW. Although Cr and Cr-Pyr reduced ADG and ADFI, BW was not affected in the Cr and Cr-Pyr broilers throughout the length of the trial.…”

Section: Discussionmentioning

confidence: 93%

Comparison of the novel compounds creatine and pyruvateon lipid and protein metabolism in broiler chickens

Chen

Wang

Kong

et al. 2011

Animal

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The effects of pyruvate (Pyr), creatine pyruvate (Cr-Pyr) and creatine (Cr) on lipid and protein metabolism were compared in broiler chickens. A total of 400 1-day-old male birds (Aconred) were allocated to four groups, each of which included four replicates (25 birds per replicate). Treatments consisted of unsupplemented basal diet (Control), basal diet containing 2% Pyr, basal diet containing 3% Cr and basal diet containing 5% Cr-Pyr. Cr-Pyr and Pyr significantly decreased the hepatic triglyceride and serum total cholesterol concentration (P , 0.01). Cr-Pyr markedly increased the serum non-esterified fatty acid and highdensity lipoprotein cholesterol concentrations (P , 0.05), whereas the expression of carnitine palmitoyl transferase I (P , 0.05) and peroxisome proliferators-activated receptor-a (P , 0.01) mRNA in the liver were both decidedly enhanced in the Cr-Pyr group. The relative leg muscle weight was higher in the Cr-Pyr group than in the control group, whereas the serum uric acid content and hepatic glutamic-oxaloacetic transaminase activity were lower in the Cr-Pyr and Cr groups (P , 0.05), respectively. Muscle insulin-like growth factor I (P , 0.05) expression was enhanced, and the myostatin (P , 0.01) mRNA level was reduced in both the Cr-Pyr and Cr groups. In addition, Cr-Pyr did not alter body weight or the feed conversion ratio. These results indicate that, compared with Pyr and Cr alone, Cr-Pyr has a bifunctional role in broiler chickens, in that it influences both lipid and protein metabolism.Keywords: creatine pyruvate, pyruvate, creatine, lipolysis, protein synthesis ImplicationsIn this study, the administration of creatine pyruvate (Cr-Pyr, a new compound, which contains pure pyruvic acid molecularly bound to pure pharmaceutical grade creatine at a concentration ratio of 40 : 60) was compared with the administration of Pyr or Cr alone for its effect on lipid and protein metabolism in broilers. The insights gained from this study will provide a better understanding of the mechanisms involved in the Cr-Pyr effect on broiler chickens. Further clarity will help the industry to avoid obesity-related problems during production and explore new ways to improve muscle growth in broilers.

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Section: Discussionmentioning

confidence: 93%

Comparison of the novel compounds creatine and pyruvateon lipid and protein metabolism in broiler chickens

Chen

Wang

Kong

et al. 2011

Animal

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“…There is also evidence that the mitochondria of the obese Zucker rat are dysfunctional. For example, these rats have a low metabolic rate and decreased reliance on fat as an energy source at rest and during exercise (6,21,22,52). In addition, the obese Zucker rat has extremely high intramuscular triglyceride content, which suggests that its muscle is incapable of normal fat oxidation (9).…”

Section: Discussionmentioning

confidence: 99%

LKB1-AMPK signaling in muscle from obese insulin-resistant Zucker rats and effects of training

Sriwijitkamol

Ivy

Christ-Roberts

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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is a key regulator of fat and carbohydrate metabolism. It has been postulated that defects in AMPK signaling could be responsible for some of the metabolic abnormalities of type 2 diabetes. In this study, we examined whether insulin-resistant obese Zucker rats have abnormalities in the AMPK pathway. We compared AMPK and ACC phosphorylation and the protein content of the upstream AMPK kinase LKB1 and the AMPKregulated transcriptional coactivator PPAR␥ coactivator-1 (PGC-1) in gastrocnemius of sedentary obese Zucker rats and sedentary lean Zucker rats. We also examined whether 7 wk of exercise training on a treadmill reversed abnormalities in the AMPK pathway in obese Zucker rats. In the obese rats, AMPK phosphorylation was reduced by 45% compared with lean rats. Protein expression of the AMPK kinase LKB1 was also reduced in the muscle from obese rats by 43%. In obese rats, phosphorylation of ACC and protein expression of PGC-1␣, two AMPK-regulated proteins, tended to be reduced by 50 (P ϭ 0.07) and 35% (P ϭ 0.1), respectively. There were no differences in AMPK␣1, -␣2, -␤1, -␤2, and -␥3 protein content between lean and obese rats. Training caused a 1.5-fold increase in AMPK␣1 protein content in the obese rats, although there was no effect of training on AMPK phosphorylation and the other AMPK isoforms. Furthermore, training also significantly increased LKB1 and PGC-1␣ protein content 2.8-and 2.5-fold, respectively, in the obese rats. LKB1 protein strongly correlated with hexokinase II activity (r ϭ 0.75, P ϭ 0.001), citrate synthase activity (r ϭ 0.54, P ϭ 0.02), and PGC-1␣ protein content (r ϭ 0.81, P Ͻ 0.001). In summary, obese insulin-resistant rodents have abnormalities in the LKB1-AMPK-PGC-1 pathway in muscle, and these abnormalities can be restored by training.acetyl-CoA carboxylase; peroxisome proliferator-activated receptor-␥ coactivator-1␣; exercise AMP-ACTIVATED PROTEIN KINASE (AMPK) is an energy-sensing enzyme that is activated by increases in AMP-to-ATP ratios through mechanisms involving allosteric modification and phosphorylation by one or more upstream AMPK kinases (AMPKKs) (11,25). AMPK is a heterotrimer that is formed by a catalytic ␣-subunit and the regulatory ␤-and ␥-subunits. There are two isoforms of the ␣-and ␤-subunits and three isoforms of the ␥-subunit (11, 25). Upon activation, AMPK switches on catabolic pathways that generate ATP, such as glucose transport and fatty acid oxidation, coupled with the inhibition of ATP-consuming (anabolic) pathways that include triglyceride and cholesterol synthesis. It has become apparent in recent years that AMPK plays a key role in mediating the acute and long-term effects of exercise on carbohydrate and fat metabolism in skeletal muscle. AMPK mediates, at least in part, exercise-stimulated increases in muscle glucose transport (3,15,34,35) and fatty acid oxidation (53, 57). The stimulatory effect of AMPK on fatty acid oxidation results from the phosphorylation and inhibition of acetyl-CoA carboxylase (ACC) by AMPK (10, 53, 59). There is evidence that AM...

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“…The conclusions were not surprising in light of the fact that muscle of lean healthy subjects predominantly uses lipid as an oxidative fuel (25,26). Kelley and Simoneau (27) extended these results to include uncomplicated obesity (28) and Ivy and colleagues (29,30) showed that obese insulin-resistant rats displayed increased glucose oxidation in skeletal muscle. The studies that used local indirect calorimetry and carbohydrate oxidation under postabsorptive conditions in type 2 diabetes and obesity seem to contradict other studies using systemic indirect calorimetry that indicated either decreased or unchanged glucose oxidation in insulin resistance.…”

Section: Randle In Reverse: Glucose Competition With Fatmentioning

confidence: 95%

Fuel selection in human skeletal muscle in insulin resistance: a reexamination.

2000

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For many years, the Randle glucose fatty acid cycle has been invoked to explain insulin resistance in skeletal muscle of patients with type 2 diabetes or obesity. Increased fat oxidation was hypothesized to reduce glucose metabolism. The results of a number of investigations have shown that artificially increasing fat oxidation by provision of excess lipid does decrease glucose oxidation in the whole body. However, results obtained with rodent or human systems that more directly examined muscle fuel selection have found that skeletal muscle in insulin resistance is accompanied by increased, rather than decreased, muscle glucose oxidation under basal conditions and decreased glucose oxidation under insulin-stimulated circumstances, producing a state of "metabolic inflexibility." Such a situation could contribute to the accumulation of triglyceride within the myocyte, as has been observed in insulin resistance. Recent knowledge of insulin receptor signaling indicates that the accumulation of lipid products in muscle can interfere with insulin signaling and produce insulin resistance. Therefore, although the Randle cycle is a valid physiological principle, it may not explain insulin resistance in skeletal muscle. Diabetes 49:677-683, 2000 I n 1963, Sir Philip Randle outlined a principle that spawned an enormous amount of research over the following 4 decades. He performed a series of experiments that were designed to test the supposition that cardiac and skeletal muscle possessed mechanisms that allowed these tissues to shift readily back and forth between carbohydrate and fat as oxidative energy sources, depending primarily on the availability of free fatty acids (FFAs). In particular, these experiments eventually focused on the biochemical mechanisms that are involved in the switch from carbohydrate to fat oxidation (1-3). The main features of the model that was developed were that increased fat oxidation in muscle would inhibit both pyruvate dehydrogenase (PDH) and phosphofructokinase by accumulation of acetyl CoA and citrate, respectively. These roadblocks placed in the glycolytic pathway would lead to increased glucose 6-phosphate concentration, inhibiting hexokinase and resulting in reduced glucose uptake and oxidation. This homeostatic mechanism became known as the glucose fatty acid cycle or the Randle cycle (Fig. 1).Insulin-deficient rat models of diabetes, as well as people with type 1 diabetes, exhibit elevated rates of lipolysis, increased plasma FFAs and triglyceride concentrations, elevated blood ketone bodies, and decreased respiratory quotients (RQs). Thus, it was hypothesized that the glucose fatty acid cycle operated under these conditions to inhibit glucose metabolism and contribute to hyperglycemia (2). Later, as the extent of insulin resistance in obese and type 2 diabetic patients was discerned, investigators took note of the association between insulin resistance and increased plasma nonesterified fatty acids (4). It has been postulated that the Randle cycle might be responsible for insulin r...

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Effects of pyruvate and dihydroxyacetone consumption on the growth and metabolic state of obese Zucker rats

Cited by 37 publications

References 15 publications

Comparison of the novel compounds creatine and pyruvateon lipid and protein metabolism in broiler chickens

Comparison of the novel compounds creatine and pyruvateon lipid and protein metabolism in broiler chickens

LKB1-AMPK signaling in muscle from obese insulin-resistant Zucker rats and effects of training

Fuel selection in human skeletal muscle in insulin resistance: a reexamination.

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