2022年2022年如何回復審稿人意見

1、精選學習資料 - - - 歡迎下載dear editor、we have studied the valuable comments from you、 the assistant editor and reviewers carefully、 and tried our best to revise the manuscript. the point to point responds to the reviewer s comments are listed as following:responds to the reviewer s comments: reviewer 1commen

2、t 1:in page 3、 line 40、 we fed rats." changed to rats were fed with.response: according to the reviewers comment、 we have corrected the sentence. furthermore、 we have had the manuscript polished with a professional assistance in writing.comment 2: page 25. the style of reference 40 is not right

3、 using initials for the first names. since this paper has been published、 the volume and page nos should be provided.response: thank you for your careful work. we have added the volume and page numbers for reference 40.reviewer 2comment:iwouldliketo thank the authors fortheir effortsinaddressing the

4、 criticisms withadditional experiments. the one criticismthat they did not address was relating to energy expenditure as the reason that the animals on the low calcium diet gained more weight. while i understand that performing this experiment will not affect the conclusion of this manuscript、 i do

5、believe that this point could be discussed in the discussion section.response: thank you for your valuable advice. based on the previous revision、 we further address the relationship between low calcium diet and energy expenditure in the section of discussion according to your thoughtful comments.精品

6、學習資料精選學習資料 - - - 歡迎下載reviewer 3comment 1 : in the text you often write:“ as previously described” . unless that pap is from your lab or one of the method paper co-authors is on the present ms this is notquite proper since the statement infers method development from your lab. there are numerous inst

7、ances likethat in the methods section; these should all be changed “ according to those described by. ”response: we are sorry for this language mistake. we have carefully corrected this phrase throughout the manuscript according to your comment.comment 2:there are still some wording、 sentence struct

8、ure and grammatical issues even in this basically wellput together ms. for example、 while authors may havebeen excited about the data you cannot start a sentence with“ excitedly” in line“ whatever ” in line 395.response: thank you very much to point out the sentence structure and grammatical issues

9、in our manuscript. according tothe comments from you and the editors、 we polished the manuscript with a professional assistance in writing、 conscientiously.comment 3:in my view a big omission in this work is ignoring the anabolic sideoflipidmetabolismas wellas thermogenesis issues. for example allan

10、imals consumed the same amount of feed but we had extra fat storage in the low ca diet groups. so where did the extra energy go. zemel et al citation 34 in similar work indicate that increased thermogenesis on the high ca diet explains the dissipation of dietary energy. further even though zemel et

11、al #34 indicated lipogenesis was enhanced in the low ca diets that was in 2000 and you shouldhave monitored expression of fas and ucpeitheras mrnaabundance oractualfas/ucp changes viaproteomicsorblottingtechniques. inany case these controlsare missing here and notemphasized in thems. casual reading

12、of thispaper would lead to the conclusion that the dietary ca effect on fat deposition is strictly a function of increased or decreased lipolysis. while lipolysis appears to be a major player、 lipogenesis and thermogenesis cannot be ignored for completeness.in fig 8 you also show a decline incampfor

13、the lowca diet. wellbeta agonists or camp enhancers regulate transcription ofadipose and liverfas inrats j biolchem 271:2307、 1996 and recently withlarge animal models hausman et al j animal science 87:1218、 2021 and halsey et al j animal science 89: 1011、 2021. in addition精品學習資料精選學習資料 - - - 歡迎下載cam

14、p levels could have been monitored. i really do not like the last sentence in the abstract line 47-50 where you state that“ low calcium-inddieutced increase in fat mass wasduetoenhancedlipogenesis mediatedbyanupregulatedcasr signalingpathway ”y ourresults here show no such thing、 this is a completel

15、y false statementbased ondataherein.correct.youshow that highca diets enhance lipolysisand lowca diets are antilipolytic.youdid not monitorlipid anabolism here at all. see also line 255-257 and lines 333-335 of your ms. response: thank you for your valuable and thoughtful comments. as you suggested

16、that the anabolic side of lipid metabolism as well as thermogenesis issues should be monitored. we really agree with your viewpoints. in the present study、 we did find that low calcium diet increased the mrna level of fatty acid synthase fas in white adipose tissue. furthermore、 the fas mrna level w

17、ere also increased in adipocytes after treatment with1、25-oh2d3 in in-vitroexperiments. however、 the increased fas mrnalevels were not affected by preventing either the nuclear vitamind receptor nvdr or calcium-sensing receptor casr、 suggesting that fas might not be involved in the casr pathway. in

18、addition、 we thought that fas played its role in fatty acid synthesis mainly in liver previously. besides、 the manuscript was required to restrict number of total words and our previous focus was on the antilolytic role of casr in the process of fat accumulation. so we ignored to provide the data of

19、 fas mrnalevels in the submitted manuscript. in the newly submitted manuscript、 we have provided the mrna levels according to your helpful suggestion.we have reported the effects ofdietary calcium on ucp2 mrnalevels in adipose tissue and ucp3 in skeletal muscle in our previous studies 1、 2. thus、 we

20、 believed that low calcium diet led to decreased thermogenesis in the present study. it was a pitythat we did not measurethe rat core temperature in those studies. the ucp2 mrna levels in adipocytes were observed to be decreased after treatment of 1、25-oh2d3. this effect was prevented by usingnvdr c

21、asr gene silencing but not by casr gene knockdown、 suggesting that ucp2 was not involved in casr pathways. in the newly submitted manuscript、 we have provided the ucp2 results.thank you for your careful reading of our manuscript. we are very sorry for our fault statement in the abstract. we have cor

22、rected it in the new manuscript.comment 4:a point that does not emerge well from the discussion is how low ca intakes result in higher intracellular ca concentrations and really the effects on fat精品學習資料精選學習資料 - - - 歡迎下載deposition in the cells in many ways are due to an increased intracellular ca lev

23、el mediated via casr expression increases and the effect of vitd3 on nvdr show infig 8. the authors must remind readers that ca levels in the blood are under hormonalregulation calcitonin、 pth and vitd3.thus when diets low in ca are consumed and blood ca decline、 pthand vitd3are called upon to mobil

24、izebone ca to replenish the blood ca. then coupled with an increase in casr more ca actually is found in at despite the fact that many would think the at ca level should decline.the reason is that tissue/circulating ca levels are not diet depended but regulated. the vast bone stores of ca will provi

25、de ample ca here especially during a study of this length. whileauthors address these issues maybe couldbe presented in a less complicated discussion.response: thankyouforyourinstructivesuggestions. weare sorryfornot describing the effect oflowcalciumdiet on intracellularcalcium concentrations media

26、ted by casr、 as wellas the impact of hormone regulation on serum calcium levels clearly. according to your helpful advice、 we have rewritten these two parts in the section of discussion. thank you again.comment 5: not all citations are in jn styleresponse: we have careful recheck and corrected the s

27、tyle of the citations according to the requirement of jn.comment 6: abstract conclusion differs from lines 255-257 and 333-335; why. response: thank you for your careful reading of our manuscript. the conclusion from lines 255-257 is about the effect of low calcium diet on serum levels of free fatty

28、 acids ffasand lipids.we considered ffaand glycerolas indicatorsoftg hydrolysis in adipose tissue. the low calcium diet caused decreased serum ffa and glycerol levels without influencinglipoprotein lipase lpl activity、 so we thought the lipolytic effect of adipose tissue to be suppressed by low calc

29、ium diet. the conclusion from lines 333-335 was about the effect of 1、25-oh2d3 whose levels were increased under low calcium conditions on lipolysis. we used the glycerol level as the indicator of tg hydrolysis in adipocytes. both the in vivo and in vitro experiments showed low calcium status caused

30、 an antilipolytic effect.精品學習資料精選學習資料 - - - 歡迎下載comment 7:line 150-153. the qrt-pcr methodology is not at all understandable as you cite a texas a&m published paper. this iscompletely insufficientwith the newly established standards on gene expression via qrt-pcr. there is no mention of efficiencies of amplifications in these data nor how the use of t