Thermogenesis and dietary requirements -
However, if the mouse decreases in body weight and lipid content is reduced, the inevitable result is then necessarily that the density of everything else found in, e. Again, only if analyzed at the total tissue level, can correct conclusions be drawn.
While this problem, i. This may sometimes be performed by cutting the tissue into small pieces, placing these in an oxygen electrode chamber e. There are, however, several problems with this methodology and its interpretation. One is that already alluded to above: when lipid amounts in the tissue are decreased, everything else, expressed per g wet weight, must necessarily be increased; the values for oxygen consumption per g tissue weight can thus be higher merely because there is more protein per g wet weight, without any recruitment having taken place.
In such preparations, it is not unlikely that what is measured is unregulated succinate oxidation occurring in damaged mitochondrial fragments in the tissue pieces. The information that can be obtained from this must necessarily be limited although again, the values will presumably be higher in samples with less lipid.
A third problem arises when this type of preparation is stimulated, e. The problem that arises is a consequence of the inability of the inner part of the tissue pieces to receive sufficient oxygen. If brown adipose tissue is stimulated with norepinephrine in situ in the animal , the NADH level decreases, as would be expected, due to the induced uncoupling of the mitochondria [ 30 ].
This uncoupling will allow for electron flow from NADH to oxygen and NADH levels will thus decrease. However, when NADH levels are followed in tissue pieces from brown adipose tissue, the levels increase.
This is because lipolysis is stimulated by norepinephrine, lipid catabolism is increased and more NADH is generated from, e. In the absence of sufficient oxygen in the tissue pieces, the electrons cannot flow to oxygen, and NADH accumulates.
Thus, the tissue pieces become hypoxic when stimulated [ 30 ] and measurement of thermogenesis in this type of preparation is therefore not meaningful. A standard method to follow changes in tissues is to analyze tissue samples for, e.
This is a natural way to work, e. A major problem is illustrated in Fig. In Fig. The relevant conditions could be several. One is what happens when the tissue goes from a dormant to an active state: blood flow increases markedly, and the tissue fills up with blood, containing red and white blood cells.
There can also be a true invasion in the form of, e. This is what may be referred to as pseudoatrophy: that the data indicate a lowering of the component of interest—but in reality this has not taken place.
The issue of pseudoatrophy. In a , the control condition is shown. The red circles represent the protein-of-interest. There are also other proteins in the tissue brown.
A value is obtained for the protein-of-interest per mg protein c , left bar. In b , a change in the physiological conditions has meant that extra components green circles have been incorporated as constituents of the tissue e.
In this situation, if the concentration of the protein-of-interest is calculated per mg protein, the result would be as that seen in c right bar : a clear decrease an atrophy.
However, if the total amount of the protein-of-interest is measured, it is unchanged d. Thus, the result in c is misleading and represents a state of pseudoatrophy. Similar outcomes may be encountered for mRNA levels. Again, the solution to the problem is to calculate the total amount of the component of interest in the tissue, to obtain physiologically relevant values.
Concerning diet-induced thermogenesis, the level of UCP1 protein attracts special attention, as it is generally considered to be the rate-limiting step for this thermogenesis. However, it is important that an antibody with high specificity is used since a large number of other mitochondrial carrier proteins have very similar molecular weights.
These antibodies cannot be used uncritically in other tissues where they can cross-react with proteins of similar molecular weight see also 3.
This issue is not only theoretical. Although not directly investigated for diet-induced thermogenesis, a confounding and apparent decrease in UCP1 per mg protein is observed in the very early phases of cold acclimation, probably due to the presence of more blood in the tissue [ 31 ].
In all these cases, it turns out that the total amount of UCP1 in the tissue is not decreased, nor is the magnitude of norepinephrine-induced thermogenesis. Thus, the decrease in UCP1 levels per mg protein leads to an erroneous conclusion concerning the thermogenic capacity of the tissue. Accordingly, if a weight-reducing agent should lead, e.
If changes in thermogenic capacity are to be estimated from a biochemical measure, UCP1 is the natural candidate. It would generally be recognized that total muscle power cannot be adequately determined only by analyzing a single sample from muscle but must include an estimate of the total amount of muscle.
Similarly, to obtain a total thermogenic estimate, the measurements should always include both UCP1 per mg protein and a measure of total protein in the depot, and only after multiplying these values can an estimate of total UCP1 and thus total thermogenic capacity be reached. However, this could be said to be not fully adequate, because only the total amount of UCP1 in one brown adipose tissue depot—normally the interscapular depot—is obtained.
The implication will then be that similar changes occur in all brown adipose tissue depots. Optimally, all brown adipose tissue depots should be measured but this is seldom realistic.
Additionally, although there is good reason to think that thermogenesis and total UCP1 protein levels correlate positively, the relationship is not always proportional, i.
To obtain a biochemical value of the thermogenic capacity of the mouse, e. For determination of UCP1 levels, we referred to it as being expressed per mg protein, when obtained from a western blot.
However, the high plasticity of brown adipocytes can make this procedure untenable. A perfect loading control would be a protein that does not change with physiological conditions, when expressed per mg protein. but there would then be no point in dividing by this value, as it would always be the same.
Reports of apparent chnages in UCP1 that are the result of physiological changes in the loading control may be encountered. Thus, presently, expressing changes in specific proteins in brown adipose tissue is best done by expressing them per mg protein—and recalculating to the total amount in the depot.
Ponceau or amido-black staining can indicate equal loading but even the pattern of these may change substantially in different physiological conditions due to the plasticity.
It is presently much more common to present data about proteins in terms of their mRNA levels rather than as protein amounts or enzymatic activity. The main reason for this is that it is technically easier, particularly if a series of different proteins are examined.
However, the apparent ease comes with problems of its own. Particularly, if UCP1 mRNA levels are used as a proxy for UCP1 protein levels, it must be remembered that UCP1 mRNA has a rapid turnover hours [ 34 ] and shows marked daily variation [ 35 ], whereas UCP1 protein has a much slower turnover days [ 36 ] and needs weeks to achieve new steady state levels.
It is therefore not surprising that there may not be a direct correlation between UCP1 mRNA levels and UCP1 protein at a given time point, if this is during a transition state; these issues have been discussed in more detail elsewhere [ 37 ].
Due to the rapid induction of UCP1 gene expression by norepinephrine released from the sympathetic nerves in the tissue and to the rapid turnover of UCP1 mRNA, the levels of UCP1 mRNA an be seen as better proxies for acute sympathetic nerve activity in the tissue than for thermogenic capacity, particularly in physiological transition states.
qPCR techniques have an immense sensitivity span. Differences in expression of a million times can in principle be detected. A change of 10 Ct values corresponds to a difference of in gene expression level, a change from 35 to 25 is thus fold different, to 15 is 1,,fold different, and Ct values below this may then approach at least 10,,fold difference in expression.
UCP1 mRNA levels that give Ct values of 20 and below are needed to produce UCP1 protein in sufficient amounts for it to induce uncoupling in isolated mitochondria. It is thus difficult to ascribe physiological significance to gene expression levels times lower i. Such low UCP1 mRNA can be detected in certain tissues under certain conditions.
However, it is important to express the UCP1 mRNA data in such a way that the absolute values are evident. Thus, in diet-induced thermogenesis studies, for thermogenic relevance, UCP1 mRNA levels should be expressed with the same units in all the different depots. Studies of gene expression are therefore often accompanied by attempts to identify a good housekeeping gene to normalize to.
In reality, this amounts to identifying a gene that does not change between conditions—but if such a gene is found, it is used to divide all data by the same constant —that should then yield a result that is identical to that obtained without normalization cf.
A further problem that may be encountered in this search is to look only at the Ct values and conclude that they are practically identical e. However, due to the logarithmic nature of the Ct values, such a difference represents a doubling of the divisor level. If there is a doubling of expression of the normalization gene, this will necessarily result in an apparent halving of the expression of the gene-of-interest, even if no such change has actually occurred.
This means in reality that the levels are expressed per mg RNA. As discussed above for protein levels, an organismal point of view should be attempted also for mRNA levels. In reality, within the limitations that half-lives etc. constitute, mRNA levels are used as indicators of enzymatic activity providing information on UCP1 thermogenic capacity , since protein amounts are generally determined by mRNA amounts.
Although this relationship is not always valid and examples where it is not can be found even in brown adipose tissue contexts [ 38 ] , this must still be the basic idea in steady states.
The normal representation of UCP1 mRNA levels is then per mg RNA or per normalizing gene. Rather, for an organismal view, the total amount of UCP1 mRNA is obtained by multiplying UCP1 mRNA levels per mg RNA with the total amount of RNA in the tissue the total amount obtained in the isolation procedure.
To obtain this value, it is therefore important also in this context to quantitatively dissect the total depot. Due to the large differences in RNA levels between different tissues, this adjustment may alter the thermogenic significance that should be given to UCP1 gene expression in different tissues.
Notably, the total amount of RNA is, e. Thus, presenting the data in this way yields a result that is physiologically more meaningful. One way to infer thermogenic adipose tissue recruitment in studies of diet-induced thermogenesis is to show immunohistochemical staining of the tissue with anti-UCP1 antibodies.
There are several problems in the interpretation of such data. One problem is that many commercial UCP1 antibodies are not sufficiently specific. The monoclonal antibody we recommend for western blots cannot be used, as it is made in mice, and secondary antibodies to this antibody therefore react with all mouse antibodies in the tissue slices.
The specificity problem can best be verified by using tissue from UCP1 KO mice as a negative control, or at least tissue pieces from a non-UCP1 expressing tissue with high mitochondrial content e.
Further problems arise not least because the tissues change their composition during recruitment. Firstly, there is the cm 2 effect discussed above Fig.
Secondly, stimulation of the tissue may increase the number of mitochondria without increasing the amount of UCP1. Although many antibodies are made against short UCP1 peptides, there is a risk that they recognize other members of the mitochondrial carrier protein superfamily. This is particularly the case because when used for immunohistochemical staining the antibodies are often added in high concentrations, increasing the risk for unspecific reactions.
There is no simply solution to this; again analysis of tissues from a UCP1 KO mouse should increase the validity of the observations. It would seem that e. in inguinal adipose tissue a population of adipocytes inherently exists where the UCP1 gene is already open for transcription when the cells are adrenergically stimulated.
This means that UCP1 gene expression is necessarily stimulated in these responsive cells; the increase in UCP1 is thus not causative of the weight loss through activated thermogenesis but is caused by the weight loss.
Due to the low initial level of UCP1 gene expression normally observed in the inguinal adipose tissue, the thermogenic capacity of the induced UCP1 is negligible, although the relative increase in UCP1 gene expression can be marked.
Why such a cell population exists in the inguinal adipose tissue is not clarified. There are methodological issues relating to the obesity, even in these measurements.
A standard experiment to demonstrate altered glucose homeostasis in obese mice versus slim mice is the glucose tolerance test.
In these experiments, a single dose of glucose is injected into the mouse often intraperitoneally. This leads to a rapid increase in blood glucose levels, and the trajectory of glucose normalization is a measure of the diabetic state Fig.
However, the injections generally given are 2 g per kg body weight. This means that a substantially greater amount of glucose is injected into an obese versus a lean mouse, often nearly twice as much. However, as the aqueous volume in which the glucose is dissolved in the body is essentially the same in the two cases, the curve for glucose disposal will necessarily be very different Fig.
Thus, at first sight, there appears to have been a very convincing improvement: when the mouse is obese, it is also pre diabetic. When it becomes leaner, the pre diabetes disappears.
In reality, this is the inevitable outcome if 2 g glucose per kg body weight is injected as it is in practically all published cases. This can be presented as a positive effect of BAT activation on improving glucose tolerance if the obesity is considered to be reduced due to BAT activity.
However, because of the procedure, this difference is either largely exaggerated or does not exist. The inherent effect of obesity on the outcome of glucose tolerance tests.
In the standard procedure, a dose of glucose proportional to body weight is injected into the mouse a. This results in a glucose tolerance test, principally as sketched in the lower curve in b. If the same body weight-paradigm for glucose dose is used for obese mice, a higher amount of glucose is injected, but it will be dissolved in practically the same amount of lean mass i.
This will thus, everything else being equal, result in the top curve in b. Note that this will necessarily occur even without any true change in glucose tolerance.
This does not mean that an obesity-induced reduction of glucose tolerance does not exist, rather that methodologically either the same dose of glucose e. This allows for the possibility to discern the true effect of obesity on the glucose tolerance test.
These issues have been discussed in several papers [ 40 , 41 ]. A much more labor-intensive but basically also more informative procedure is the euglycemic, hyperinsulinemic clamp, where a high saturating dose of insulin is continuously injected into the mouse and the amount of infused glucose needed to compensate for the glucose disposal is measured.
However, routinely, also here the result that will initially be expressed as moles of glucose per animal per min will be expressed divided by body weight.
Again, inevitably, the obese mouse will present with an apparently decreased glucose disposal capacity, whereas the lean mouse will appear to have a greater capacity. Thus, also in these experiments, the result should be presented without division, i.
It is very likely that the phenomenon of diet-induced thermogenesis does exist and that it is located mainly or entirely in BAT and is due to UCP1 recruitment and activation. With time, it may indeed prove possible to recruit diet-induced thermogenesis to ameliorate obesity.
However, it is of paramount importance for confidence in studies that underlie such undertakings that the measurements, results, and interpretations that constitute progress in the field avoid deceptive pitfalls.
We hope that the compilations of possible pitfalls above will facilitate development of a deeper physiological understanding in this important field.
If not, translational studies will have a high risk of failing, as they would be based on unfounded conclusions from preclinical studies. Maxwell GM, Nobbs S, Bates DJ Diet-induced thermogenesis in cafeteria-fed rats: a myth?
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Correspondence to Jan Nedergaard or Barbara Cannon. Program in Molecular Medicine, UMass Chan Medical School, Worcester, MA, USA. Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4. The images or other third party material in this chapter are included in the chapter's Creative Commons license, unless indicated otherwise in a credit line to the material.
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Reprints and permissions. Nedergaard, J. Diet-Induced Thermogenesis: Principles and Pitfalls. In: Guertin, D. eds Brown Adipose Tissue. Fact Checked. Capsaicin in chili peppers enhances thermogenesis. Certain spices can increase thermogenesis. Video of the Day.
Green Tea. Green tea has also been shown to increase thermogenisis. Coconut Oil. Coconut oil has been shown to inhibit fat deposition. Diets high in protein are the most thermogenic. Westerterp-Plantenga; August "Pharmacological Research:" Medium-Chain Fatty Acids: Functional Lipids for the Prevention and Treatment of the Metabolic Syndrome; K.
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Diet-induced thermogenesis DIT refers to require,ents increase in metabolic rate Healthy snacks to curb appetite follows the ingestion of food, as well as changes adn with chronic reuirements in the Thermogenesis and dietary requirements level of energy intake i. the plane of nutrition. The term DIT therefore includes phenomena such as the specific dynamic action SDA or thermic effect TE of food, and is synonymous with the heat increment of feeding HIF used by agricultural nutritionists see previous chapter for dicusssion of terminology. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. Claudio Maffeis, Yves Schutz, Alessandra Grezzani, Silvia Talent nurturing and progression pathways, Giorgio Thermogenesis and dietary requirements, Luciano Tatò, Meal-Induced Thermogenesis and Obesity: Is a Fat Meal a Risk Anc for Fat Thermogenesis and dietary requirements ane Children? Diet composition, in wnd fat intake, has been suggested to be a risk factor for obesity in humans. Several mechanisms may contribute to explain the impact of fat intake on fat gain. One factor may be the low thermogenesis induced by a mixed meal rich in fat. In a group of 11 girls Each girl repeated the test with a different, randomly assigned menu HF or LF 1 week after the first test.Thank you for visiting nature. Rewuirements are using a browser version with aand support for CSS. To obtain the best experience, dietxry recommend ajd use a requiremsnts up to Healthy snacks to curb appetite browser or turn off Themrogenesis mode in Internet Explorer.
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Each Thsrmogenesis was dietaary on a chair in Energy conservation methods semisupine position in a quiet room in which the temperature and humidity were controlled to within After allowing the subjects to adjust to the experimental setup for 20 min, baseline data of gas-exchange variables and the splanchnic circulation were recorded while resting for 20 min.
The subjects completed a mm visual analogue scale VAS questionnaire to assess their hunger and fullness before the test drink.
A mL cocoa-flavored drink was divided into ten mL cups. After performing baseline measurements, the subjects swallowed the ten mL test drinks over a 5-min experimental period in three ways.
In the control trial, subjects swallowed one mL test drink every 30 s. In the long-duration taste stimulation trial taste trialsubjects kept the mL test drink in their mouth for 30 s without chewing, and then swallowed it; stimulation was taste only.
In the chewing stimulation trial chewing trialsubjects chewed the mL test drink for 30 s at a frequency of once per second, and then swallowed it; stimulation was both taste and chewing. Gas-exchange variables and the splanchnic circulation were measured until 90 min after swallowing the test drink.
The subjects consumed the same mL cocoa-flavored drink Calorie Mate Can, Otsuka, Japan; kcal; protein 7. Subjects scored their hunger and fullness on a mm VAS before the test drink. The subjects marked a tick on the line to indicate their feeling, with the score corresponding to the distance in millimeters from the left starting point of the line to the tick.
Oxygen uptake ·VO 2carbon dioxide output ·VCO 2and respiratory exchange ratio RER were measured using a gas analyzer AES, Minato Medical Science, Japan on a breath-by-breath basis before and after the test drink. The average data every 15 min and the last 15 min of the resting baseline were used for the analysis.
Energy expenditure at resting baseline REE and after the test drink was calculated using the abbreviated Weir equation 28 :. DIT was calculated from the postprandial increments in energy expenditure above the resting baseline.
Accumulation for DIT over 90 min was calculated area under the curve AUC using the trapezoidal rule. Substrate oxidation was calculated from ·VO 2 and ·VCO 2 using the following formulas 29 :.
Protein oxidation was assumed to be Accumulation for substrate oxidation over 90 min was calculated from AUC using the trapezoidal rule. The heart rate HR and the mean blood velocities MBVs and vessel diameters of the celiac artery CA and superior mesenteric artery SMA were measured.
HR was determined using the electrocardiograph MEG, Nihon Kohden, Japan. Simultaneous pulsed and echo Doppler ultrasound flowmetry was used to measure the MBVs and vessel diameters of the CA and SMA, as in previous studies of our research group 212230 A curved-array Doppler-scan probe was operated at a pulsed Doppler frequency of 3.
After obtaining these signals for measuring MBV for 1 min, a cross-sectional image of the vessel was recorded for 30 s. This was repeated every 5 min.
The B-mode images sent from the Doppler monitor were recorded to enable later measurement of the vessel diameters using image-editing software ImageJ 1. The spectra of the MBV signals were analyzed offline with our own Doppler signal processing software, and beat-by-beat MBV values were calculated.
MBV was determined by averaging the ten largest values in each minute for 1 min every 5 min in order to eliminate data variations originating from the abdominal movement associated with respiration 30 The blood flows BFs in the CA and SMA were calculated using the following formula:.
Accumulation for splanchnic BF in the CA and SMA over 90 min was calculated from incremental AUC using the trapezoidal rule. All statistical analyses were performed with SPSS IBM SPSS Statistics A P value of less than 0. One-way analysis of variance ANOVA was used to compare hunger and fullness scores before the test drink, baseline data of gas-exchange variables, substrate oxidation, and splanchnic circulation, and accumulation for DIT, substrate oxidation, and splanchnic BF over 90 min after consuming the test drink among all trials.
Two-way repeated ANOVA was used to examine effects of trials and time on time course data. There was no difference among trials after the intake. The time courses of the gas-exchange variables ·VO 2·VCO 2and RER are shown in Fig. The gas-exchange variables at the resting baseline did not differ significantly among the trials.
Significant interaction of trial and time was found for ·VO 2. The duration over which ·VO 2 was significantly greater than the resting baseline was longer in the chewing trial than in the control and taste trials.
Significant interaction of trial and time was found for ·VCO 2. RER did not differ significantly among the trials. Time courses of changes in gas-exchange variables and diet-induced thermogenesis DIT in the control, taste, and chewing trials.
Circles, triangles, and squares denote data from the control, taste, and chewing trials, respectively. resting baseline in each trial. A significant interaction of trial and time was found for DIT Fig. DIT was significantly greater in the taste and chewing trials than in the control trial; these differences continued until 90 min after the test drink between chewing and control trials, and was evident at 45—75 min between taste and control trials.
The duration over which DIT was significantly greater than the resting baseline was longer in the taste and chewing trials than in the control trial. The time courses of the substrate oxidations protein, fat, and carbohydrate are shown in Fig.
Significant interaction of trial and time was found for protein oxidation. Protein oxidation was significantly greater in the chewing trial than in the control trial at 45—60 min after the test drink.
Fat and carbohydrate oxidation did not differ significantly among the trials. Time courses of changes in substrate oxidation protein, fat, and carbohydrate in the control, taste, and chewing trials. The time courses of the splanchnic circulation MBV, diameter, BF for the CA and SMA are shown in Fig.
The splanchnic circulation at the resting baseline did not differ significantly among the trials. Significant interaction of trial and time was found for CA MBV. CA MBV was significantly greater in the chewing trial than in the taste trial at 30—45 min after the test drink.
Significant interaction of trial and time was found for CA diameter. CA diameter did not differ significantly among the trials. Significant interaction of trial and time was found for CA BF. CA BF was significantly greater in the taste and chewing trials than in the control trial; these differences was evident at 15—30 min and 60—75 min between taste and control trials, and was evident at 15—30 min between chewing and control trials.
SMA MBV, SMA diameter, and SMA BF did not differ significantly among the trials. Time courses of changes in splanchnic circulation in the control, taste, and chewing trials.
CA celiac artery, SMA superior mesenteric artery, MBV mean blood velocity, BF blood flow. The DIT that accumulated over the 90 min after swallowing the test drink was significantly greater in the chewing trial than in the control and taste trials [control trial, 3.
The accumulated substrate oxidation for protein, fat, and carbohydrate did not differ significantly among trials [protein oxidation: control trial, 3. The accumulated CA BF was significantly greater in the taste and chewing trial than in the control trial [control trial, Diet-induced thermogenesis DITsubstrate oxidation, and postprandial splanchnic circulation accumulated over the min period immediately after consuming the test drink.
Lines join individual values, and symbols circles, triangles, and squares indicate mean values.
: Thermogenesis and dietary requirements| Mechanisms of Diet-Induced Thermogenesis | Encyclopedia MDPI | The effects of oral stimuli i. Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4. Duodenal Lipid Sensing Activates Vagal Afferents to Regulate Non-Shivering Brown Fat Thermogenesis in Rats. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Nat Commun 11 1 Maxwell GM, Nobbs S, Bates DJ Diet-induced thermogenesis in cafeteria-fed rats: a myth? |
| We Recommend | Thus, the requirementss from pictures such as these would Thermogenesis and dietary requirements dietqry that the tissue has become recruited, e. Sakata, T. Online ISSN: Print ISSN: Jéquier, E. Targeted disruption of histamine H1-receptor attenuates regulatory effects of leptin on feeding, adiposity, and UCP family in mice. Zucker rats. |
| What are Thermogenic Supplements? | It is also termed the thermic effect of food or the specific dynamic action of food. A Publisher Correction to this article was published on 23 December Case Studies. Contrasting data are available on the extent to which diet composition and fat intake play important roles in the development of childhood obesity 12 — Targeted disruption of histamine H1-receptor attenuates regulatory effects of leptin on feeding, adiposity, and UCP family in mice. |
| Diet induced thermogenesis | Leptin-deficient mice are not hypothermic, they are anapyrexic. Article CAS PubMed Google Scholar Faul, F. The methods for examination of these models would appear straightforward, but experience shows that particularly the obesity that is induced in both models makes the interpretation of the results difficult, often leading to claims that diet-induced thermogenesis has been demonstrated under conditions where this is not the case. This article is cited by Pre-exercise isomaltulose intake affects carbohydrate oxidation reduction during endurance exercise and maximal power output in the subsequent Wingate test Naoko Onuma Daisuke Shindo Kentaro Yamanaka BMC Sports Science, Medicine and Rehabilitation The evolving view of thermogenic fat and its implications in cancer and metabolic diseases Xinpeng Yin Yuan Chen Qiang Xu Signal Transduction and Targeted Therapy MDPI and ACS Style MDPI and ACS Style AMA Style Chicago Style APA Style MLA Style. Curr Opin Clin Nutr Metab Care ; 9 : — Lab Interpretation. |
neugierig, und das Analogon ist?
Mir scheint es die prächtige Idee