0649病弱名無しさん (ﾜｯﾁｮｲ a516-IoJz [122.196.177.121])2017/11/18(土) 23:28:54.14ID:JSdk9JrA0 ケトン体が癌を増悪させる、転移させるって言ってる論文は、どれくらいの重みがあるん？ 癌が増悪、転移してる人達は、皆ケトン体モリモリかよｗ んなわけないんで、どういうこと？ 0650じゃろにます ◆klokDYkn/k (ﾜｯﾁｮｲ a34b-rBqA [115.30.198.190])2017/11/19(日) 08:53:01.07ID:v6AnH/b00 結局のところ、九官鳥くんが持ってきた論文は基本的には invitroの研究とガンのMCT高発現から乳酸とケトンを使ってる！という推測です。 だから常に乳酸とケトンはセットになっているわけです。 そもそもケトンでガンが発生するというエビデンスはありませんし、発ガン後の経過についても かんたんにできる動物実験ですらケトーシスで腫瘍が増大するという結果の出た論文はありません。 逆にケトーシスで腫瘍が縮小した論文はあります。 これが現時点でわかっているすべてです。 九官鳥くんは「生命の神秘」を重視するならせめてケトーシスで腫瘍増大した動物実験のエビデンスを出しましょう。 0651じゃろにます ◆klokDYkn/k (ﾜｯﾁｮｲ a34b-rBqA [115.30.198.190])2017/11/19(日) 08:54:58.45ID:v6AnH/b00 今日の宿題です。 0652病弱名無しさん (ｱｳｱｳｲｰ Sa99-x/r4 [36.12.83.51])2017/11/19(日) 09:08:49.28ID:yTuY3IC/a>>650 全然読んでませんやん ケトン食でマウスでは食事療法を行った実験群で最初に癌の成長が遅くなるが、その後、成長速度が増し、統制群よりも増長する In an experiment on mice, the tumors in the diet-treated group initially grew less but later tumor growth accelerated and exceeded that of the that of the control group
>他の実験によると、癌の成長が小さくなるのは、体重が減るからで、食事療法とは関係なかった。 Other experiments show that a reduction of tumor growth is seen if the animals lose weight – independent from the kind of diet
https://www.ncbi.nlm.nih.gov/pubmed/17313687/0654病弱名無しさん (ｱｳｱｳｶｰ Sac9-w7ui [182.251.245.46])2017/11/19(日) 09:14:22.73ID:0elkKrVya>>650 人とネズミの違いもある。 0655病弱名無しさん (ｱｳｱｳｲｰ Sa99-x/r4 [36.12.83.51])2017/11/19(日) 09:19:47.38ID:yTuY3IC/a Low carbohydrate diet and ketogenic diet. Different forms of this diet exist, some with a moderate reduction of carbohydrates some with a reduction to about 10% of total energy intake with the aim of inducing ketosis. Schmidt et al. (23) published a pilot study on 16 patients with advanced cancer, on a diet with a maximum of 70 g carbohydrates per day, for an intended eight weeks. Two patients died, three did not accept the diet and three had progressive disease. Quality of life was assessed in five patients who finished the study. Emotional function and sleep quality was better while other parameters remained stable or deteriorated. The authors argue that this was due to the advanced stage of their cancer. Side-effects of the diet were fatigue and constipation 0656病弱名無しさん (ｱｳｱｳｲｰ Sa99-x/r4 [36.12.83.51])2017/11/19(日) 09:20:37.27ID:yTuY3IC/a A retrospective analysis of five children with tuberous sclerosis on a ketogenic diet because of untreatable epilepsy did not reveal any influence on brain tumors (24). A case report of two children with brain tumors on a ketogenic diet describes a reduction of glucose uptake in PET-CT. One girl survived for several months without progression (25).
In an older study, a ketogenic diet with high amounts of omega-3-fatty acids was fed enterally to patients with cachexia from cancer. The authors did not describe a positive effect on cachexia or on the course of disease (26).
Pre-clinical data are ambiguous. Some show a reduction of tumor. Yet some in vitro as in vivo experiments, gave warnings as to the safety of this diet. In vitro data showed that cancer cells not only adapt to the situation but develop mutations and characteristics of stem cells. One hypothesis is that the diet puts the tumor under stress and thus selects for resistance and malignancy. In an experiment on mice, the tumors in the diet-treated group initially grew less but later tumor growth accelerated and exceeded that of the control group (28, 29, 30, 31).
糖質をこれほど摂らなければ、本来これほどのカロリーも必要ないのでは ないのではと感じてしまいますが。 0675病弱名無しさん (ｽﾌｯ Sd03-/Aq4 [49.104.4.43])2017/11/19(日) 15:13:57.41ID:ASVwuUund>>674 おっと、計算したら脂質と、タンパク質半分程度でした。 倍にしておいてくださいw 0676病弱名無しさん (ｱｳｱｳｲｰ Sa99-x/r4 [36.12.73.247])2017/11/19(日) 15:46:53.63ID:OiHPLFhLa Effect of diclofenac on SLC16A3/MCT4 by the Caco-2 cell line - ScienceDirect
https://www.sciencedirect.com/science/article/pii/S1347436716300076 モノカルボン酸輸送担体MCT4はがん細胞に高発現しており，がん患者の予後不良因子であることが知られている．そのため，MCT4は新たながん治療の標的として期待されている． MCT4そのものの機能を簡便に評価することのできるツールは，MCT4を標的とした医薬品を開発する上で有用である．これまでMCT4の機能解析はXenopus laevis oocyte発現系を用いて行われてきたが，我々は新たに， Caco-2細胞において典型的なMCT基質である乳酸がMCT4を介して取り込まれる可能性を示した．したがってCaco-2細胞はMCT4の機能を解析するための簡便なツールであることが示唆された． 今後，MCT4の機能に影響を与える化合物の探索を進めて行きたいと考えている．本研究が，がん患者の予後を改善する一助となることを期待している． 0677病弱名無しさん (ｱｳｱｳｲｰ Sa99-x/r4 [36.12.73.247])2017/11/19(日) 15:50:06.85ID:OiHPLFhLa Oxidative stress in cancer associated fibroblasts drives tumor-stroma co-evolution: A new paradigm for understanding tumor metabolism, the field effe... - PubMed - NCBI
https://www.nature.com/articles/onc20134540688じゃろにます ＝殘lokDYkn/k (ﾜｯﾁｮｲ a34b-rBqA [115.30.198.190])2017/11/19(日) 20:47:34.14ID:v6AnH/b00 そろそろコピペ卒業して自分の言葉で語りませんかね？ 0689病弱名無しさん (ｱｳｱｳｲｰ Sa99-x/r4 [36.12.77.35])2017/11/19(日) 21:00:48.83ID:IP35oBlLa Cancer metabolism, stemness and tumor recurrence: MCT1 and MCT4 are functional biomarkers of metabolic symbiosis in head and neck cancer. - PubMed - NCBI
We propose that oxidative stress is a key hallmark of tumor tissues that drives high-energy metabolism in adjacent proliferating mitochondrial-rich cancer cells, via the paracrine transfer of mitochondrial fuels (such as L-lactate and ketone bodies). 0690病弱名無しさん (ｱｳｱｳｲｰ Sa99-x/r4 [36.12.77.35])2017/11/19(日) 21:03:34.26ID:IP35oBlLa Autophagy and senescence in cancer-associated fibroblasts metabolically supports tumor growth and metastasis, via glycolysis and ketone production: Cell Cycle: Vol 11, No 12
http://www.tandfonline.com/doi/abs/10.4161/cc.207180691病弱名無しさん (ｱｳｱｳｵｰ Sa93-x/r4 [119.104.11.3])2017/11/19(日) 21:24:37.02ID:NgAaZQfja Oncogenes induce the cancer-associated fibroblast phenotype: Metabolic symbiosis and “fibroblast addiction” are new therapeutic targets for drug discovery: Cell Cycle: Vol 12, No 17
Catabolic fibroblasts donate the necessary fuels (such as L-lactate, ketones, glutamine, other amino acids, and fatty acids) to anabolic cancer cells, to metabolize via their TCA cycle and oxidative phosphorylation (OXPHOS). This provides a simple mechanism by which metabolic energy and biomass are transferred from the host microenvironment to cancer cells. Recently, we showed that catabolic metabolism and “glycolytic reprogramming” in the tumor microenvironment are orchestrated by oncogene activation and inflammation, which originates in epithelial cancer cells. Oncogenes drive the onset of the cancer-associated fibroblast phenotype in adjacent normal fibroblasts via paracrine oxidative stress. This oncogene-induced transition to malignancy is “mirrored” by a loss of caveolin-1 (Cav-1) and an increase in MCT4 in adjacent stromal fibroblasts, functionally reflecting catabolic metabolism in the tumor microenvironment. 0692病弱名無しさん (ｱｳｱｳｵｰ Sa93-x/r4 [119.104.11.3])2017/11/19(日) 21:33:14.24ID:NgAaZQfja More specifically, we show that the enzymes required for ketone body production are highly upregulated within cancer-associated fibroblasts. This appears to be mechanistically controlled by the stromal expression of caveolin-1 (Cav-1) and/or serum starvation. In addition, treatment with ketone bodies (such as 3-hydroxy-butyrate, and/or butanediol) is sufficient to drive mitochondrial biogenesis in human breast cancer cells.
