Creatine supplementation alters insulin secretion and glucose homeostasis in vivo

Rooney, Kieron; Bryson, Janet M.; Phuyal, Jenny L.; Denyer, Gareth; Caterson, Ian D.; Thompson, Campbell

doi:10.1053/meta.2002.31330

Cited by 42 publications

(57 citation statements)

References 25 publications

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“…Possibly, the mechanism through which creatine affects glucose metabolism is the stimulation of insulin pancreatic secretion, since, although glucose is the greatest stimulator of insulin secretion, it can also be induced by proteins and amino acids. The role of creatine as stimulator of insulin secretion has been demonstrated in in vitro (18)(19) as well as in vivo studies, confirming the very same alterations (16)(17) . Nevertheless, this long-term insulin hypersecretion may induce also to insulin resistance (20) , which has probably not been previously studied in creatine supplementation.…”

Section: Introductionsupporting

confidence: 56%

“…It has been demonstrated in vitro (18)(19) that creatine affects the metabolism of the carbohydrates when directly stimulates the insulin secretion of isolated pancreatic islets. Such fact was confirmed in vivo (16) in a work studying the creatine supplementation in rats in order to observe the long-term effects in the glucose transportation and storage in the skeletal muscle. Moreover, it showed high insulin secretion and alteration in the glucose homeostasis after eight weeks of supplementation when compared with the controls.…”

Section: Discussionmentioning

confidence: 62%

“…Although it has been demonstrated in vivo (16) that chronic supplementation of creatine leads to hypersecretion of insulin, the fact is that the long-term hypersecretion of insulin may also induce insulin-resistance (20) , which is the topic of the present study. Having this hypothesis as starting point, we investigated the effects of this hypersecretion of insulin facing chronic supplementation of creatine, searching for evidences of insulin-resistance in rats weekly followed during seven, 14, 21 and 28 days.…”

Section: Discussionmentioning

confidence: 93%

“…It has also been demonstrated that creatine increases the muscular storages of glycogen (13) . Glycogen resynthesis (14) and increase of the glucose-carrier protein (15) have been observed in the creatine supplementation, altering the regulation of the glucose metabolism (16)(17) . Possibly, the mechanism through which creatine affects glucose metabolism is the stimulation of insulin pancreatic secretion, since, although glucose is the greatest stimulator of insulin secretion, it can also be induced by proteins and amino acids.…”

Section: Introductionmentioning

confidence: 99%

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Resistência à insulina com a suplementação de creatina em animais de experimentação

Costallat¹,

Miglioli²,

Silva³

et al. 2007

Rev Bras Med Esporte

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Introduction and objective:Creatine supplementation has been used in order to improve muscular performance. This substance affects glucose metabolism and stimulates the in vitro as well as the in vivo insulin secretion. Nevertheless, long-term insulin hypersecretion may also induce insulin resistance. The present work analyzed the effects of creatine oral supplementation in order to evaluate the possibility of occurrence of resistance to in vivo insulin. Methods: Forty-eight Wistar rats (24 female/ 24 male) were divided in two groups of 24 (control and study) and subdivided in six groups of eight. They were fed with standard food during four weeks, having water ad libitum. Moreover, the study group received dietetic supplement of creatine (0.4 g creatine for 30 ml of water per rat / day). In the 7 th , 14 th , 21 st and 28 th day of the experiment, 12 rats were anesthetized (sodium thiopental 0.15 mL/ 100 g) after six hour-fasting, being submitted to intravenous insulin tolerance test (0.5 mL of 30% regular human insulin and 70% saline solution). The blood samples were collected from the tail veins of the rats, in the basal, three, six, nine, 12 and 15 minutes after insulin administration times. The glucose measurement was performed through the glucose oxidase method. The study was previously approved by the Research Ethics Committee of CCMB-PUC-SP. Results: The mean of the glucose decrease constant (K ITT ) was calculated through the formula 0.693/ T 1/2 . The study group, when compared with the control group, presented insulin resistance at day 21 (p < 0.0004) and day 28 (p < 0.0001). Conclusion: This study shows that extended creatine supplementation may lead to insulin resistance. Besides that, it should be carefully used in individuals with glucose metabolism disturbances.

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Section: Introductionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Resistência à insulina com a suplementação de creatina em animais de experimentação

Costallat¹,

Miglioli²,

Silva³

et al. 2007

Rev Bras Med Esporte

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“…This dose (1% of diet by weight ϭ 0.01 ϫ 30 g/day per 350 g rat ϭ ϳ0.85 g Cr ⅐ kg Ϫ1 ⅐ day Ϫ1 ) is in excess of that routinely used by humans during a Cr-loading regimen (20 g/day per 70 kg person ϭ 0.3 g ⅐ kg Ϫ1 ⅐ day Ϫ1 ). Unfortunately, we were not able to reproduce the even modest 6-20% increase in [Cr] i of rat muscle observed previously by some (26,31,32) but not by others (21). The reasons for the lack of response are unclear but may be related to the extremely high doses (up to 5% in the diet) used previously.…”

Section: Discussionmentioning

confidence: 56%

Muscle creatine uptake and creatine transporter expression in response to creatine supplementation and depletion

Brault

Abraham

Terjung

2003

Journal of Applied Physiology

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The total creatine pool size [Crtotal; creatine (Cr) + phosphocreatine (PCr)] is crucial for optimal energy utilization in skeletal muscle, especially at the onset of exercise and during intense contractions. The Crtotal likely is controlled by long-term modulation of Cr uptake via the sodium-dependent Cr transporter (CrT). To test this hypothesis, adult male Sprague-Dawley rats were fed 1% Cr, their muscle Crtotal was reduced by ∼85% [1% β-guanidinoproprionic acid (β-GPA)], or their muscle Crtotal was repleted (1% Cr after β-GPA depletion). Cr uptake was assessed by skeletal muscle 14C-Cr accumulation to Cr and PCr by using hindlimb perfusion, and CrT protein content was assessed by Western blot. Cr uptake rate decreased with dietary Cr supplementation in the white gastrocnemius (WG; 45%) only. Depletion of muscle Crtotal to ∼15% of normal increased Cr uptake in the soleus (21%) and red gastrocnemius (22%), corresponding to 70–150% increases in muscle CrT content. In contrast, the inherently lower Cr uptake rate in the WG was unchanged with depletion of muscle Crtotal even though CrT band density was increased by 230%. Thus there was no direct relationship between apparent muscle CrT abundance and Cr uptake rates. However, Cr uptake rates scaled inversely with decreases in muscle Crtotal in the high-oxidative muscle types but not in the WG. This implies that factors controlling Cr uptake are different among fiber types. These observations may help explain the influence of initial muscle Crtotal, time dependency, and variations in muscle Crtotal accumulation during Cr supplementation.

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Urinary type II collagen neoepitope as an outcome measure for relapsing polychondritis

Kraus

Stäbler

et al. 2003

Arthritis & Rheumatism

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Herein we describe the case of a man who was diagnosed as having relapsing polychondritis (RP) when he was 18 years of age and was treated over the course of 2 years with numerous immunosuppressive agents, including tumor necrosis factor ␣ (TNF␣) inhibitors. His respiratory symptoms were refractory to treatment. Serum and urine samples were obtained periodically for measurement of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) levels, antitype II collagen (anti-CII) antibodies, and urinary type II collagen neoepitope (uTIINE) levels. The uTIINE assay is specific for collagenase cleavage products CII present in urine. ESRs and CRP levels varied widely but were rarely normal. Anti-CII antibody titers were high initially and decreased slowly and steadily for a year following the start of immunosuppressive medication, remaining low throughout the remainder of the patient's monitored disease course. The uTIINE levels were elevated prior to the initiation of TNF␣ inhibitors. Upon initiation of etanercept, they decreased abruptly to normal and stayed nearly normal. The uTIINE levels rose abruptly again upon discontinuation of TNF␣ inhibitor treatment. The dramatic decline in CII degradation, coincident with the administration of the TNF␣ inhibitors, suggested that this treatment dramatically reduced the chondritis. Serum levels of Th1 cytokines (interferon-␥, interleukin-12 [IL-12], and IL-2) paralleled changes in uTIINE levels, while those of Th2 cytokines (IL-4, IL-5, IL-6, and IL-10) showed little or no association with disease state or uTIINE levels.These results indicate that RP might be a Th1-mediated disease process. Moreover, the uTIINE assay appears to provide an objective measure of the severity of chondritis that could assist clinical decisions regarding adjustments of steroid and other immunosuppressive therapy. This outcome measure merits investigation in a broader spectrum of RP patients.

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Creatine supplementation alters insulin secretion and glucose homeostasis in vivo

Cited by 42 publications

References 25 publications

Resistência à insulina com a suplementação de creatina em animais de experimentação

Resistência à insulina com a suplementação de creatina em animais de experimentação

Muscle creatine uptake and creatine transporter expression in response to creatine supplementation and depletion

Urinary type II collagen neoepitope as an outcome measure for relapsing polychondritis

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