what to do if you drink too much red bull

  • Journal List
  • Anatol J Cardiol
  • v.19(5); 2018 May
  • PMC6280269

Anatol J Cardiol. 2018 May; 19(5): 326–333.

Long-term consumption of energy drinks induces biochemical and ultrastructural alterations in the middle musculus

Camelia Munteanu

Department of Molecular Biology and Biotechnology, Babes-Bolyai Academy; Cluj-Napoca-Romania

Corina Rosioru

Department of Molecular Biological science and Biotechnology, Babes-Bolyai University; Cluj-Napoca-Romania

Corneliu Tarba

Section of Molecular Biology and Biotechnology, Babes-Bolyai University; Cluj-Napoca-Romania

Camelia Lang

Department of Molecular Biology and Biotechnology, Babes-Bolyai University; Cluj-Napoca-Romania

Abstract

Objective:

Energy drinks (EDs) target immature and active individuals and they are existence marketed as enhancers of energy, concentration, and physical and cognitive operation. Their long-term consumption raises serious health concerns related to cardiovascular events. Hither we investigate the effects of long-term Red Bull® consumption and its combination with booze on sure biochemical parameters and the ultrastructure of the myocardium.

Methods:

Male Wistar rats were categorized into four groups and given different treatments via oral assistants. The Control (C) grouping received tap water, the Red Bull (RB) grouping received 1.v ml/100 thou body weight of Red Bull, the ethanol group (E) received 0.486 mg/100 g body weight of ethanol, and the Red Bull and ethanol (RBE) received a combination of the two beverages for 30 days. In the last vi days of the experiment, the animals were tested for their physical functioning by conducting a weight-loaded forced swim test. Immediately after pond exhaustion, the animals were sacrificed nether anesthesia and samples of the heart muscle were harvested for ultrastructural and biochemical analyses.

Results:

Our results showed a significant increment in the heart glucose and glycogen concentrations in the RB and RBE groups. Total cholesterol concentration significantly decreased in the RBE and RB groups. Total protein concentration and ALT and AST activities increased in all groups. The biochemical changes were accompanied by ultrastructural alterations.

Conclusion:

Based on these results, we recommend that athletes and active persons should avoid the long-term consumption of the Blood-red Balderdash ED and, particularly, its combination with alcohol.

Keywords: energy drinks, Red Bull, ethanol, heart muscle

Introduction

Energy drinks (EDs) target young and physically agile individuals. They contain large quantities of active components such every bit caffeine, taurine, and niacin. EDs are branded as agents or enhancers of energy, concentration capacity, and physical and mental performance (1). However, the consumption of EDs, particularly in large quantities, is associated with the occurrence of cardiovascular events such as cardiac arrhythmias, chest pain, hypertension, and even sudden cardiac decease (2). Every bit such, the condom of the long-term consumption of EDs is questionable.

The explosive increase in the consumption of EDs over the past years has led the scientific customs to investigate the influence of such products on human health and to identify the reasons for their consumption. Additionally, the past years have witnessed an increase in the incidence of negative effects associated with the consumption of EDs, the virtually common adverse furnishings noticed being the nervous, cardiovascular, and gastrointestinal effects.

The risks are even college if EDs are combined with alcohol. Several studies have investigated the effect of EDs in combination with alcohol and have shown that EDs significantly reduce the immediate furnishings of ethylic intoxication, which may lead to an increased consumption of alcoholic drinks (3). Ferreira et al. (4) have shown that, when combined with booze, Carmine Bull attenuates the perception of alcoholic intoxication.

In full general, the brusk- and long-term effects of the consumption of EDs are controversial. Several studies have addressed the brusque-term effects of EDs, targeting specific components of EDs and not EDs in their entirety, and have reported positive short-term effects induced by these specific components. For example, it has been shown that caffeine activates AMP-activated protein kinase (AMPK), which is a key enzyme that coordinates several signaling pathways that are involved in maintaining cellular energy homeostasis (v). Additionally, caffeine causes sympathomimetic effects, intensifying centre activity and increasing blood pressure (six).

Information technology has also been proven that taurine is an indirect regulator of oxidative stress in the myocardium, stabilizing the cellular membranes by straight interacting with phospholipids. Information technology exhibits various biological activities such every bit a positive influence on the calcium kinetics as well as the protection of the cardiac function and is a modulator of poly peptide kinases and phosphatases in cardiomyocytes. Farther, it maintains the normal contractile function of the heart musculus (seven) and reduces arterial pressure (eight).

Some EDs (v-60 minutes ENERGY shots, Monster, Rockstar Energy, and Red Bull) incorporate niacin (vitamin B3) in doses above the daily recommended intake. Niacin has positive effects in restoring a good for you lipid profile and delaying the progression of atherosclerosis (9). It has been used for more than half a century in the treatment of lipid disorders, such as abnormally elevated concentrations of LDL, not-HDL cholesterol, triglycerides, and lipoproteins and low concentrations of HDL (ix, ten).

In fact, most studies accept shown that a moderate consumption of EDs over a short catamenia of time improves the cognitive and psychomotor capacities (11). However, some studies have also highlighted the occurrence of negative effects past the consumption of EDs, such as an increase in the heart rate, and systolic and diastolic pressures and a decrease in the cerebral blood flow (12, xiii).

Finally, the long-term effects of the consumption of EDs on unlike systems have been comparatively studied, and those of such drinks on the cardiovascular system are unknown. However, based on known data (run across the preceding paragraph), our hypothesis is that the consumption of EDs represents a serious cardiac hazard factor. The aim of this report was to investigate the effects of the chronic consumption of an ED (Cherry Bull) and of its combination with alcohol and to highlight their influence on sure biochemical parameters and the ultrastructure of the myocardium.

Methods

Chemicals

All reagents used in this written report were of analytical grade and were purchased from Sigma-Aldrich Chemie GmbH, Deutschland. The Cherry-red Bull ED was bought from a local market.

Animals and treatments

The study was conducted on male Wistar rats, which were kept under standard weather condition and had gratis access to water and food. Experiments were performed according to the national regulations and were approved past the Institutional Ethics Commission (Registration no. 17928/2017).

Twenty-8 albino male Wistar rats, weighing 182.xi±4.7 g, were divided into the following iv groups, each with 7 animals: the Control (C), Blood-red Balderdash (RB), ethanol (Eastward), and Cerise Bull and ethanol (RBE). All animals received a standard diet. The C grouping had ad libitum access to tap h2o, the RB group were orally administrated with ane.v ml/100 g body weight of Cherry Balderdash in drinking water daily, for thirty days, and the East group received 0.486 mg/100 g trunk weight of ethanol daily. The RBE group received both Cherry Bull and ethanol in equivalent concentrations with each of the other two treated groups.

In the concluding 6 days of the experiment, the animals were tested for their physical performance by conducting a weight-loaded forced swim exam. The animals were forced to swim to exhaustion with a load of 10% of their torso weight attached to their tails. Each rat was considered to have reached exhaustion when it remained submerged for ≥5 s. H2o temperature varied between 28°C and 30°C, and none of the animals were affected by hypothermia.

After 30 days of treatment, immediately after burnout, the animals were killed by exsanguination under anesthesia. Samples of serum and heart musculus were harvested for biochemical and ultrastructural analyses, including the measurements of total middle glucose, glycogen, cholesterol and poly peptide concentrations; in improver, serum and heart musculus ALT and AST activities were measured.

Biochemical analyses

The full glucose concentration was determined using the Somogy Nelson colorimetric analysis (xiv, xv). Glycogen concentration was determined using the Montgomery method (sixteen) modified by Lo et al. (17). Total cholesterol was assayed using ferric chloride (eighteen). Total poly peptide concentration was determined using the Bradford colorimetric analysis (19) with the Bradford "ready-to-use" reagent. AST and ALT activities were analyzed using the Reitman and Frankel photocolorimetric analysis (xx).

Ultrastructural analyses

For electron microscopy analyses, the myocardium specimens were fixed in 2.7% glutaraldehyde and 2% osmium tetroxide, successively washed in phosphate buffer, and dehydrated in increasing concentrations of acetone. They were so embedded in Epon, and slices were cut at l-90 nm using a Leica UC6 Ultra microtome on a drinking glass pocketknife. The sections were assorted and visualized at 80 kV using a TEM JEOL JEM-1010. Images were obtained with a Mega Wiew III camera (21).

Statistical assay

All data are presented as mean±standard difference (SD). For statistical analysis of the effects of different treatments, a one-way analysis of variance with Dunnett's test was conducted. All data were analysed using GraphPad Prism version 6 for Windows (GraphPad Software Inc., La Jolla, CA, USA). Significance was considered at values of p<0.05.

Results

Biochemical results

The effects of Cerise Balderdash, ethanol, and their combination on glucose and glycogen concentrations in the heart muscle are shown in Figure 1. These results revealed that glucose concentration increased in all treated groups, but this was significant only in the RBE grouping (RBE, one.233±0.3867 vs. C, 0.6699±0.2759; p=0.0217*) (Fig. 1a). A clear increase in the glycogen concentration (Fig. 1b) occurred in the RB group (RB 2.946±one.ii vs. C, one.077±0.4033; p=0.0019**).

An external file that holds a picture, illustration, etc.  Object name is AJC-19-326-g001.jpg

Changes induced past the combined physical effort (swimming examination) and consumption of Cherry Bull and/or ethanol on (a) glucose and (b) glycogen concentrations in the myocardium. The results are presented as mean±SD. P<0.05* and P<0.01** vs. C. C - command; RB - Red Bull; East - ethanol, RBE - Cherry-red Balderdash and ethanol. n=7 in all groups

The concentration of cholesterol was significantly decreased in all treated groups (RB, two.144±0.3724 vs. C seven.365±3.224; p=0.0004***; East, 2.874±1.071 vs. C 7.365±3.224; p=0.0017**; RBE, 2.264±0.6763 vs. C, 7.365±3.224; p=0.0004***; Fig. 2a).

An external file that holds a picture, illustration, etc.  Object name is AJC-19-326-g002.jpg

Variations in (a) total cholesterol and (b) protein concentrations in the myocardium later on concrete try (pond test) and consumption of Red Balderdash and/or ethanol. The results are presented as mean±SD. P<0.05*, P<0.01** and P<0.01*** vs. C. C - control; RB - Red Balderdash; Eastward - ethanol; RBE - Red Bull and ethanol. n=seven in all groups

Our results showed a slight increment in the myocardial poly peptide concentration in all treated groups, being significant in the Due east group (E, 105.3±3.883 vs. C, 98.23±4.852; p=0.0475*) (Fig. 2b).

AST and ALT activities increased in the myocardium and decreased in the serum in all groups (Fig. iii). The increase in the ALT action in the myocardium was pregnant only in the RB group (RB, 144.5±25.06 vs. C, 115.1±13.43; p=0.0203*).

An external file that holds a picture, illustration, etc.  Object name is AJC-19-326-g003.jpg

The combined furnishings of physical effort (pond test) and consumption of Red Bull and ethanol on (a) serum AST, (b) serum ALT, (c) myocardium AST, and (d) myocardium ALT activities. The results are presented as mean±SD. P<0.05* and P<0.01** vs. C. C - command; RB - Carmine Balderdash; Eastward - ethanol; RBE - Cherry-red Bull and ethanol. northward=7 in all groups

Ultrastructural alterations

The most serious ultrastructural modifications observed in the heart tissue of rats in the Due east group (Fig. 4a- 4d) were those that indicated the onset of alcoholic cardiomyopathy (a loose organization of myofibrils, and large spaces between myocytes occupied by several bloated mitochondria with dilated cristae). The morphological alterations induced in the middle muscle by EDs were very similar to those induced past ethanol (Fig. 4e and 4f).

An external file that holds a picture, illustration, etc.  Object name is AJC-19-326-g004.jpg

Ultrastructure of the ventricular myocardium. (a) Control group: tightly packed intermyofibrillar mitochondria (Mt) surrounded by parallel bands of myofibrils (Myo), with contractile filaments organized in sarcomeres. Numerous lipid droplets (L) are visible in the proximity of mitochondria. Intercalated disks (ID) are visible at the limit between two side by side cells. Bar, 2 µm. (b) Control group: tightly packed intermyofibrillar and subsarcolemmal mitochondria (Mt) with visible cristae are surrounded by parallel bands of myofibrils (Myo), with contractile filaments organized in sarcomeres. Lipid droplets (L) are visible in the proximity of mitochondria. Intercalated disks (ID) are visible at the limit between ii adjacent cells. BV, blood vessel; PM, plasma membrane. Bar, ii µm. (c) Ethanol-treated group: collagen fibers (C) are abundant in the intercellular space; lysis areas (arrowheads) are visible in the spaces occupied by mitochondria; some mitochondria have altered cristae. Bar, v µm. (d) Ethanol-treated group: enlarged spaces between myofibrils are occupied past numerous mitochondria, some showing altered cristae; in contrast, subsarcolemal mitochondria population is reduced, and lysis areas (arrowheads) are visible. Bar, 5 µm. (e) Ruddy Balderdash-treated grouping: the intermyofibrillar spaces are enlarged, with numerous lysis areas (arrowheads); numerous mitochondria take altered cristae. Bar, 5 µm. (f) Red Bull-treated group: numerous lysis areas (arrowheads) are nowadays in the intermyofibrillar spaces; several mitochondria show disrupted cristae. Bar, v µm. (g) Red Bull and ethanol-treated group: disorganized intercalated disks (ID); numerous mitochondria with disrupted cristae (arrowheads). Bar, ii µm. (h) Cherry Bull and ethanol-treated group: numerous vesicles that seem to be filled with glycogen (arrowheads) in the intermyofibrillar spaces, mitochondria having destroyed cristae (Mt), and disorganized intercalated disks (ID). Bar, 5 µm

Discussion

This study shows, for the first time, that the long-term consumption of EDs, individually or in combination with ethanol, causes biochemical and ultrastructural alterations in the centre muscles.

Our results revealed that both Red Bull and ethanol increased glucose and glycogen concentrations in the myocardium. In the RB group, the increment in the glucose and glycogen concentrations was acquired past two ingredients of ED, caffeine and taurine. Commonly, caffeine causes calcium release from the intracytoplasmic stores (22) and activates AMPK via calcium/Calmodulin-dependent protein kinase kinase-β (CaMKK) (23). AMPK promotes the uptake and use of glucose in the cardiomyocytes (24). Besides, AMPK either inhibits glycogen synthesis via the phosphorylation of glycogen synthase or activates glycogen degradation via the phosphorylation of glycogen phosphorylase (25). However, the chronic activation of AMPK, as probably happened in our written report, may increase glycogen synthesis by increasing the glucose uptake and the germination of glucose-6-phosphate. This induces the allosteric activation of glycogen synthase that can overcome inhibitory phosphorylation by AMPK (26). Moreover, it has been reported that taurine increases glucose uptake, glycolysis, and glycogen synthesis in the middle of adult rats (27).

In our study, ethanol led to a slight increase in glucose and glycogen concentrations. Ethanol decreases the sensitivity to insulin, which is mediated in the centre musculus by tumour necrosis cistron-α (TNFα) and/or interleukin-six (IL-six), inducing the activation of Jun North-terminal kinases, which inhibits the Akt-AS160-GLUT4 signaling pathway (28). As such, the glucose concentration should accept decreased. We cannot provide an caption of these results, and at that place is no study on this topic in the literature. However, ultrastructural modifications shown in Figure 4 led us to consider that the Krebs cycle was not correctly operation and, consequently, the glucose metabolism in the myocardium was afflicted.

The combined administration of Cherry-red Balderdash and ethanol produced a significant increase in the glucose concentration, which was expected because the independent administration of each of these components increased the glucose concentration in the myocardium.

Glycogen is a vital molecule for the normal functioning of the myocardium. It is necessary for the ontogenetic development of the heart, because it supplies the necessary energy for the growth and development of the organ (29). In the mature organ, glycogen is found in small quantities, furnishing energy to the excito-usher system. A large quantity of glycogen is beneficial but nether ischemic conditions (30). Glycogen accumulation in the myocardium favours the incidence of pre-excitation syndrome (31). Several studies have reported an association of the EDs and/or alcohol with the occurrence of negative effects at the cardiovascular level (palpitations, cardiac arrhythmias, hypertension and even sudden cardiac death) (2, 32); therefore, we cannot exclude the possibility that these effects were connected to glycogen accumulation in the myocardium.

Cholesterol concentration significantly decreased in all groups. This result tin in turn be a crusade of the myocardial dysfunctions reported in the chronic consumption of EDs and alcohol. A role of cholesterol is to stiffen the cellular membranes and maintain the shape of cells by forming "bridges" (lipid rafts) in the regions where the membrane proteins are expressed (33). Additionally, cholesterol controls the membrane fluidity, and, consequently, plays an important function in the the cholesterol to phospholipid ratio (34). The molar ratio of cholesterol to phospholipids in plasma membranes is commonly maintained merely below unity (35). Therefore, reducing the cholesterol concentration may lead to membrane destabilization, which may in plow affect cellular metabolism in the myocardium.

The decrease in the cholesterol concentration induced by Red Bull might have been due to the elevated content of taurine and/or niacin present in the ED. This modify is somewhat expected because both taurine and niacin are used in the prevention and cure of atherosclerosis (36, 37). More precisely, taurine reduces serum cholesterol (38) and niacin reduces serum cholesterol and triglycerides and increases HDL concentration (39).

Decreased cholesterol in the myocardium following chronic ethanol treatment has likewise been reported past Godfrey et al. (40) and Hu et al. (41), but no one has ever explained these results and the physiological significance of the phenomenon is unknown.

The combined assistants of Red Bull and ethanol induced an fifty-fifty college reduction of cholesterol in the myocardium than the contained assistants of the 2 components.

Our results show a slight increase in the myocardial protein concentration in all treated groups, being meaning in the E group. The slight increase in the protein concentration observed after the administration of Crimson Bull could be due to the high content of vitamin B6. A dose of Ruddy Bull sold in Romania contains 250% of the recommended B6 daily dose. Vitamin B6 is an essential cofactor in the functioning of over 140 enzymes required for the synthesis, degradation, and interconversion of amino acids (42).

The formation of protein adducts could be an explanation for the significant increment in the protein concentration in the E grouping observed in our study. Enquiry has shown that alcohol causes the accumulation of protein adducts in the hepatic, nervous, and muscular tissues, aggravating the ethanol-induced toxicity in these tissues (43). In a study by Worrall et al. (44), increased amounts of reduced acetaldehyde poly peptide adducts, unreduced-acetaldehyde, and malondialdehyde-acetaldehyde were institute in the cardiac tissue of rats after 6 weeks of alcohol treatment. Furthermore, a previous study has shown that adducts formed by acetaldehyde with proteins stimulate the germination of mRNA responsible for the synthesis of collagen and expression of connective tissue proteins (45).

AST and ALT activities increased in the myocardium and decreased in the serum following all treatments. According to the ultrastructural alterations caused past Blood-red Balderdash and ethanol, the activities of these membrane integrity markers were expected to be increased in the serum. However, our results are consistent with those of Mihailovic et al. (46), who reported an increase in the AST action with unchanged ALT activity in the heart muscle later a 10-24-hour interval treatment with ethanol. Our results testify that Crimson Bull had the same detrimental effects as ethanol, at least in the middle muscle. Furthermore, the combination of Red Bull and ethanol had synergistic and/or complementary effects on AST activeness.

The most serious ultrastructural alterations observed in the eye tissue of rats treated with ethanol (Fig. 4c and 4d) are those that bespeak the onset of alcoholic cardiomyopathy. As pointed out past De Leiris et al. (47), human subjects and beast models exposed to chronic ethanol consumption undergo functional and structural alterations in the heart tissue. Oxidative stress induces lipid peroxidation, poly peptide oxidation, reduces the GSH content of mitochondria, and disturbs calcium homeostasis, impairing the contractile chapters of the eye muscle. The organelles also show modified structures with disorganized cristae, resulting in altered oxidative metabolism. An excellent work of Tsiplenkova et al. (48) gives a detailed inventory of the damages caused by ethanol in alcoholic cardiomyopathy, such every bit the amending of mitochondrial membranes including organelle swelling and loss of cristae. These authors also noticed an increase in the number of mitochondria with myocytes, in which the space occupied by mitochondria was larger than that occupied by myofibrils. This is consistent with our observation of enlarged intermyofibrilar spaces filled with mitochondria. Interestingly, we also found that the subsarcolemal mitochondria population was reduced, while numerous lysis areas were present.

In addition, nosotros noticed collagen deposits in the intercellular space, which has as well been reported past Urbano-Marquez and Fernandez-Sola (49) in human patients with alcoholic cardiomyopathy.

Whether such altered cardiomyocytes may end in apoptosis or in necrosis remains unclear; however, apoptosis, or even a combination of apoptosis and necrosis, seems to produce myocyte loss in alcoholic cardiomyopathy (50).

While cardiomyocyte alterations induced past booze consumption are well documented, in that location is very petty bear witness, if whatever, concerning ultrastructural alterations induced by EDs in the heart muscle. In some myocytes of the RB group, the myofibril organisation showed a loose construction and the infinite betwixt them was occupied by several large (swollen) mitochondria displaying a rarefied matrix and dilated cristae, which led to the supposition that oxidative metabolism was affected. All these morphological alterations correlated with measured biochemical alterations in glucose, glycogen, and cholesterol concentrations and AST and ALT activities reported in our study. The exaggerated proliferation of mitochondria ("mitochondriosis") in-between narrowed myofibrils was likewise reported past Tsiplenkova et al. (48), as a characteristic of alcoholic cardiomyopathy.

In the myocytes of the RBE group, the cumulated effects of ED and ethanol were even more dramatic, with an increase in the lysis areas, majority of myofibrils without a regular (parallel) arrangement, myofibrils with a function of them fragmented, and several mitochondria with rarefied structures and dilated cristae. Numerous vesicles were nowadays in the intermyofibrillar spaces, probably filled with glycogen, as has been previously reported (49) in alcoholic cardiomyopathy. These structural alterations too support the biochemical changes measured in our written report. Several myocytes had hypochromic nuclei with irregular borders, and the intercalated disks were fragmented and dehiscent.

Written report limitations

Our experimental groups were relatively pocket-size but allowed for the statistical processing of results. Further, the duration of further experiments should exist extended to provide better insights inon the long-term furnishings of using EDs, and to highlight possible adaptive mechanisms to their components. In addition, nosotros used just ane ED. Therefore, we consider that boosted studies are needed using several such drinks, especially because they have unlike compositions.

Conclusion

Our results explain, to a sure extent, the symptoms described in the literature for those who consume EDs in large quantities or for a long period of time. We particularly refer to glycogen accumulation in the myocardium, which tin disrupt the cardiac action and may favor the occurrence of tachycardia, palpitations, cardiac arrhythmias, hypertension, and even death (two). The lowering of cholesterol concentration may, in plow, be a crusade of myocardial dysfunctions reported in the literature following the chronic consumption of EDs and alcohol. Athletes, every bit well as active individuals, should avert both the consumption of EDs and their consumption in combination with alcohol. Our results showed that EDs produce morphological changes in the heart muscle similar to those produced by ethanol. Further inquiry, on different EDs equally a whole and on dissever components is necessary to securely understand their detrimental effects and the mechanisms by which they are produced.

Footnotes

Conflict of interest: None declared.

Peer-review: Externally peer-reviewed.

Authorship contributions: Concept – C.1000., C.50.; Pattern – C.Thou., C.R., C.Fifty.; Supervision – C.L.; Fundings – Internal resource of Faculty of Biological science and Geology; Materials – C.R., C.L.; Data collection &/or processing – C.M., C.L.; Analysis &/or interpretation – C.Yard., C.R., C.T., C.L.; Literature search – C.1000., C.L.; Writing – C.1000., C.R., C.T., C.50.; Critical review – C.M., C.R., C.T., C.L.

References

ane. Enriquez A, Frankel DS. Arrhythmogenic furnishings of free energy drinks. J Cardiovasc Electrophysiol. 2017;28:711–seven. [PubMed] [Google Scholar]

two. De Sanctis V, Soliman Due north, Soliman AT, Elsedfy H, Di Maio S, El Kholy M, et al. Caffeinated free energy drinkable consumption among adolescents and potential health consequences associated with their use:a meaning public wellness hazard. Acta Biomed. 2017;88:222–31. [PMC free article] [PubMed] [Google Scholar]

3. Verster JC, Aufricht C, Alford C. Energy drinks mixed with alcohol:misconceptions, myths, and facts. Int J Gen Med. 2012;v:187–98. [PMC costless article] [PubMed] [Google Scholar]

iv. Ferreira SE, de Mello MT, Pompéia Southward, de Souza-Formigoni ML. Furnishings of energy drink ingestion on alcohol intoxication. Alcohol Clin Exp Res. 2006;30:598–605. [PubMed] [Google Scholar]

5. Zheng G, Qiu Y, Zhang QF, Li D. Chlorogenic acrid and caffeine in combination inhibit fat aggregating by regulating hepatic lipid metabolism-related enzymes in mice. Br J Nutr. 2014;112:1034–40. [PubMed] [Google Scholar]

6. Higgins JP, Tuttle TD, Higgins CL. Free energy beverages:content and rubber. Mayo Clin Proc. 2010;85:1033–41. [PMC costless article] [PubMed] [Google Scholar]

7. Schaffer SW, Jong CJ, Ramila KC, Azuma J. Physiological roles of taurine in heart and musculus. J Biomed Sci. 2010;17(Suppl one):S2. [PMC gratuitous article] [PubMed] [Google Scholar]

8. El Idrissi A, Okeke E, Yan Ten, Sidime F, Neuwirth LS. Taurine regulation of blood force per unit area and vasoactivity. Adv Exp Med Biol. 2013;775:407–25. [PubMed] [Google Scholar]

9. Julius U. Niacin equally antidyslipidemic drug. Can J Physiol Pharmacol. 2015;93:1043–54. [PubMed] [Google Scholar]

x. Garg A, Sharma A, Krishnamoorthy P, Garg J, Virmani D, Sharma T6, et al. Role of niacin in current clinical do:a systematic review. Am J Med. 2017;130:173–87. [PubMed] [Google Scholar]

11. Duncan MJ, Hankey J. The effect of a caffeinated energy drinkable on various psychological measures during submaximal cycling. Physiol Behav. 2013;116-117:60–5. [PubMed] [Google Scholar]

12. Grasser EK, Dulloo AG, Montani JP. Cardiovascular and cerebrovascular effects in response to Carmine Bull consumption combined with mental stress. Am J Cardiol. 2015;115:183–ix. [PubMed] [Google Scholar]

thirteen. Elitok A, Oz F, Panc C, Jarikaya R, Sezikli Southward, Pala Y, et al. Acute furnishings of Red Bull energy potable on ventricular repolarization in salubrious young volunteers:a prospective report. Anatol J Cardiol. 2015;15:919–22. [PMC free commodity] [PubMed] [Google Scholar]

14. Nelson Due north. A photometric adaptation of the Somogy method for the determination of glucose. J Biol Chem. 1944;153:375–80. [Google Scholar]

15. Somogyi K. A new reagent for determination of sugars. J Biol Chem. 1945;160:61–8. [Google Scholar]

16. Montgomery R. Determination glycogen. Arch Bioch Biophys. 1957;67:378–86. [PubMed] [Google Scholar]

17. Lo South, Russel JC, Taylor AW. Determination of glycogen in small tissue samples. J Appl Physiol. 1970;28:234–6. [PubMed] [Google Scholar]

18. Zlatkis A, Zak B, Boyle AJ. A new method for the direct determination of serum cholesterol. J Lab Clin Med. 1953;41:486–92. [PubMed] [Google Scholar]

xix. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of poly peptide utilizing the principle of poly peptide-dye binding. Anal Biochem. 1976;72:248–54. [PubMed] [Google Scholar]

xx. Reitman South, Frankel S. A colorimetric method for the decision of serum glutamic oxalacetic and glutamic pyruvic transaminases. Am J Clin Pathol. 1957;28:56–63. [PubMed] [Google Scholar]

21. Kuo J. Electron Mycroscopy Methods and Protocols. Crawley: Humana Press; 2007. pp. xix–35. 67-107. [Google Scholar]

22. Kong H, Jones PP, Koop A, Zhang Fifty, Duff HJ, Chen SR. Caffeine induces Ca2+release by reducing the threshold for luminal Ca2+activation of the ryanodine receptor. Biochem J. 2008;414:441–52. [PMC free article] [PubMed] [Google Scholar]

23. Fogarty Southward, Hawley SA, Green KA, Saner N, Mustard KJ, Hardie DG. Calmodulin-dependent poly peptide kinase kinase-βactivates AMPK without forming a stable circuitous:synergistic effects of Ca2+and AMP. Biochem J. 2010;426:109–eighteen. [PMC costless article] [PubMed] [Google Scholar]

24. Daskalopoulos EP, Dufeys C, Beauloye C, Bertrand 50. AMP-activated Protein Kinase. In: Cordero MD, Viollet B, editors. AMPK In Cardiovascular Diseases. Switzerland: Springer International Publishing; 2016. pp. 179–201. [Google Scholar]

26. Hunter RW, Treebak JT, Wojtaszewski JFP, Sakamoto K. Molecular Mechanism by Which AMP-Activated Poly peptide Kinase Activation Promotes Glycogen Aggregating in Musculus. Diabetes. 2011;60:766–74. [PMC free article] [PubMed] [Google Scholar]

27. Lampson WG, Kramer JH, Schaffer SW. Potentiation of the actions of insulin by taurine. Can J Physiol Pharmacol. 1983;61:457–63. [PubMed] [Google Scholar]

28. Lang CH, Derdak Z, Wands JR. Strain-dependent differences for suppression of insulin-stimulated glucose uptake in skeletal and cardiac musculus by ethanol. Alcohol Clin Exp Res. 2014;38:897–910. [PMC gratis article] [PubMed] [Google Scholar]

29. Pederson BA, Chen H, Schroeder JM, Shou West, DePaoli-Roach AA, Roach PJ. Aberrant Cardiac Development in the Absence of Heart Glycogen. Mol Jail cell Biol. 2004;24:7179–87. [PMC free commodity] [PubMed] [Google Scholar]

30. Depre C, Vanoverschelde JL, Taegtmeyer H. Glucose for the heart. Circulation. 1999;99:578–88. [PubMed] [Google Scholar]

31. Kishnani PS, Chen YT. Disorders of Sugar Metabolism. In: Rimoin DL, Pyeritz RE, Korf BR, editors. Emery and Rimoin's Principles and Practice of Medical Genetics. sixth ed. Academic Printing; 2013. p. i.p. 35. [Google Scholar]

32. Rotstein J, Barber J, Strowbridge C, Hayward South, Huang R, Godefroy SB. Energy Drinks:An Cess of the Potential Health Risks in the Canadian Context. Int Food Take chances Anal J. 2013;iii:1–29. [Google Scholar]

33. Van Meer G, Voelker DR, Feigenson GW. Membrane lipids:where they are and how they behave. Nat Rev Mol Cell Biol. 2008;9:112–24. [PMC complimentary commodity] [PubMed] [Google Scholar]

34. Lange Y, Ye J, Steck TL. How cholesterol homeostasis is regulated by plasma membrane cholesterol in excess of phospholipids. Proc Natl Acad Sci USA. 2004;101:11664–7. [PMC free article] [PubMed] [Google Scholar]

35. Lange Y, Swaisgood MH, Ramos BV, Steck TL. Plasma membranes contain half the phospholipid and ninety% of the cholesterol and sphingomyelin in cultured human fibroblasts. J Biol Chem. 1989;264:3786–93. [PubMed] [Google Scholar]

36. Xu YJ, Arneja AS, Tappia PS, Dhalla NS. The potential health benefits of taurine in cardiovascular disease. Exp Clin Cardiol. 2008;13:57–65. [PMC gratis commodity] [PubMed] [Google Scholar]

37. Chen W, Guo JX, Chang P. The effect of taurine on cholesterol metabolism. Mol Nutr Food Res. 2012;56:681–90. [PubMed] [Google Scholar]

38. Ruparelia North, Digby JE, Choudhury RP. Effects of niacin on atherosclerosis and vascular function. Curr Opin Cardiol. 2011;26:66–seventy. [PMC gratuitous commodity] [PubMed] [Google Scholar]

39. Barter PJ. The Causes and Consequences of Low Levels of High Density Lipoproteins in Patients with Diabetes. Diabetes Metab J. 2011;35:101–six. [PMC costless article] [PubMed] [Google Scholar]

40. Godfrey J, Jeanguenin L, Castro Northward, Olney JJ, Dudley J, Pipkin J, et al. Chronic voluntary ethanol consumption induces favourable ceramide profiles in selectively bred booze-preferring (P) rats. PLoS One. 2015;x:e0139012. [PMC costless article] [PubMed] [Google Scholar]

41. Hu C, Ge F, Hyodo E, Arai Thou, Iwata Due south, Lobdell H, quaternary, et al. Chronic ethanol consumption increases cardiomyocyte fatty acid uptake and decreases ventricular contractile function in C57BL/6J mice. J Mol Cell Cardiol. 2013;59:xxx–xl. [PMC free commodity] [PubMed] [Google Scholar]

42. Dakshinamurti S, Dakshinamurti K. Vitamin B6. In: Zempleni J, Suttie JW, Gregory JF 3, et al., editors. Handbook of Vitamins. 5th ed. Boca Raton FL USA: CRC Press, Taylor and Francis; 2013. pp. 315–sixty. [Google Scholar]

43. Niemelä O. Distribution of ethanol-induced protein adducts in vivo:relationship to tissue injury. Free Radic Biol Med. 2001;31:1533–eight. [PubMed] [Google Scholar]

44. Worrall S, Richardson PJ, Preedy VR. Experimental heart muscle damage in alcohol feeding is associated with increased amounts of reduced- and unreduced-acetaldehyde and malondialdehyde-acetaldehyde protein adducts. Addict Biol. 2000;5:421–seven. [PubMed] [Google Scholar]

45. Ren J, and Wold LE. Mechanisms of alcoholic heart affliction. Ther Adv Cardiovasc Dis. 2008;2:497–506. [PubMed] [Google Scholar]

46. Mihailovic D, Nikolic J, Bjelakovic BB, Stankovic BN, Bjelakovic G. Morphometric and biochemical characteristics of short-term effects of ethanol on rat cardiac musculus. Exp Toxicol Pathol. 1999;51:545–seven. [PubMed] [Google Scholar]

47. De Leiris J, De Lorgelir M, Boucher F. Ethanol and cardiac function. Am J Physiol Heart Circ Physiol. 2006;291:H1027–8. [PubMed] [Google Scholar]

48. Tsiplenkova VG, Vikhert AM, Cherpachenko NM. Ultrastructural and histochemical observations in homo and experimental alcoholic cardiomyopathy. J Am Coll Cardiol. 1986;8(1 Suppl A):22A–32A. [PubMed] [Google Scholar]

49. Urbano-Márquez A, Fernández-Solà J. Effects of alcohol on skeletal and cardiac muscle. Muscle Nerve. 2004;30:689–707. [PubMed] [Google Scholar]

50. Piano MR. Alcoholic cardiomyopathy:incidence, clinical characteristics, and pathophysiology. Chest. 2002;121:1638–l. [PubMed] [Google Scholar]


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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6280269/

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