不能胖才是大麻煩
Adipose tissue grows by two mechanisms: hyperplasia (cell number increase) and hypertrophy (cell size increase).
We all have a genetic predisposition to the amount of fat mass that we can safely achieve..Some folks have a very limited ability to recruit new adipose cells to store excess lipids in the subcutaneous adipose tissue. The recruitment of new adipose cells is known as Adipogenesis.
Adipogenesis is the process of cell differentiation by which pre-adipocytes become adipocytes. Once these folks can no longer recruit new adipose cells to store excess lipids during times of over-feeding, their existing adipocytes (fat cells) in their fat mass, their adipocytes grow in cell size and they reach a point where they become hypertrophic.
Their adipocytes (fat cells) become very inflamed, very insulin resistant. They start leaking all kinds of inflammatory markers into the circulation. These adipocytes (fat cells) become so insulin resistant that they can no longer properly regulate the flow of fatty acids and glycerol from storage. There is an excess spill-over of fatty acids to the liver. These excess fatty acids are re-esterfied in the liver to triglycerides. These excess fatty acids and triglycerides cause extreme insulin resistance in the liver. They also cause fatty liver. There is a dramatic rise in circulating triglycerides (lipids). These excess lipids also end up stored in the pancreas and other organs causing lipotoxicity. Welcome to T2 diabetes.
"Lipotoxicity is a metabolic syndrome that results from the accumulation of lipid intermediates in non-adipose tissue, leading to cellular dysfunction and death. The tissues normally affected include the kidneys, liver, heart and skeletal muscle. Lipotoxicity is believed to have a role in heart failure, obesity, and diabetes, and is estimated to affect approximately 25% of the adult American population."
https://en.wikipedia.org/wiki/Lipotoxicity .
Folks that have metabolically health fat mass have adipose tissue that grows by hyperplasia, increase in cell number..
Adiponectin is a very important hormone that is secreted by our adipose tissue..Adiponectin is very insulin sensitizing...also increases our metabolic rate...increases fatty acid oxidation...preserves pancreatic beta-cells...adiponectin promotes glucose-stimulated insulin secretion (GSIS), prevents apoptosis (cell death), and enhances the viability of pancreatic beta-cells under a variety of conditions.
Once you have dysfunctional adipose tissue, your adipocytes release LESS adiponectin and more leptin..Adiponectin is very anti-inflammatory...Leptin is very PRO-inflammatory.
LOW blood adiponectin levels are VERY indicative of T2 diabetes and fatty liver, many other diseases.
Small healthy fat cells release very high levels of adiponectin, very low levels of leptin..
I would need to try and write a few posts about adiponectin, T2D and fatty liver..
Here is a good article on adiponectin:
"Ever since its initial discovery, adiponectin has inspired widespread interest. Readily detectable in blood, stable upon collection and relatively inert to the method of collection and diurnal changes, its levels inversely correlate with multiple metabolic disorders and related diseases. Adiponectin can therefore serve as a potent clinical biomarker in humans and rodents. From the 10,000 studies over the past two decades since its discovery, it is widely appreciated that adiponectin exerts pleiotropic metabolic effects. Adiponectin sensitizes peripheral tissues to insulin and protects against inflammation and apoptosis."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773837/ .
obesity wiki 在 農民教主碎碎念 Facebook 的最佳貼文
等一下坐車時再讀。 C15 C17 很有趣。
C15 :(Wiki)
Pentadecanoic acid is a saturated fatty acid. Its molecular formula is CH3(CH2)13COOH. It is rare in nature, being found at the level of 1.2% in the milk fat from cows.[2] The butterfat in cows milk is its major dietary source[3]
C17:(Wiki)
Heptadecanoic acid, or margaric acid, is a saturated fatty acid. Its molecular formula is CH3(CH2)15COOH. It occurs as a trace component of the fat and milkfat of ruminants,[2] but it does not occur in any natural animal or vegetable fat at high concentrations.
心血管代謝疾病:超越卡路里的影響
高糖加上高脂飲食,或許才是增加心血管代謝疾病風險最主要的原因.
高糖加上高脂飲食透過影響大腦相關
獎勵系統(reward system)及腸道菌態平衡(gut microbiome),擾亂能源平衡系統(Energy balance).
Pathways and mechanisms linking dietary components to cardiometabolic disease: thinking beyond calories.
obesity reviews:2018 May 14.
doi: 10.1111/obr.12699.
Conclusion
1.Evidence suggests that consumption of n-6 fatty acids
results in lower cardiometabolic risk factors/risk compared
with isocaloric amounts of SFA. However, differences
exist between individual SFA, and the food matrix needs to be considered; e.g. dairy foods such
as cheese and yogurts are associated with reduced cardiometabolic risk. More research is needed to clarify the differences among the individual SFA and SFAcontaining
foods.
2.Evidence strongly suggests that consumption of
fructose-sweetened, HFCS-sweetened or sucrosesweetened beverages increases cardiometabolic risk factors/risk compared with isocaloric amounts of
starch. More research is needed comparing the metabolic
effects of SSB versus sugar in solid food and sugar
in solid food versus refined or whole grain starch.
3.There is currently insufficient evidence that a highCHO
diet affects weight gain or weight loss to a different
extent than a high-fat diet. Susceptibility to weight
gain when consuming diets high in refined CHO/glycaemic load may be affected by the metabolic status of the individual (i.e. glucose tolerance/insulin
sensitivity). More studies focused on strategies to prevent
weight regain in weight-reduced subjects are
needed.
4.RCTs ranging from 4 weeks to 3 years in duration
demonstrate that consumption of aspartame does not
promote body weight gain in adults. Well-controlled
and long-term RCTs in adults are warranted to assess
the effects of saccharin, acesulfame K and steviol glycosides on body weight and other health outcomes. More
studies to assess the effects of all types of NNSs in children
are needed.
a• Continued research on the following topics could provide
important insights and strategies for slowing the
obesity epidemic.
b• The high-sugar, high-fat palatable Western diet
could be perturbing both sides of the energy balance
equation through effects on brain regions associated
with reward and/or on the gut microbiome.
c• Susceptibility to weight gain may be affected by exposure
to sugar and/or NSS during critical periods
of development from pre-conception to adult life
obesity wiki 在 農民教主碎碎念 Facebook 的最佳解答
058
French paradox 還能再扯上一大堆解釋,但都只是偏是能解釋法國人會比較瘦。
法國人傳統上有很多的,優良的飲食習慣
例如,一天只會吃上最多三餐,不會怎麼吃零食
例如,吃東西只在餐桌間
例如,慢食,享受食物
例如,法國人沒有強烈的早餐慨念,而是 break fast (打破斷食)/ small lunch(小午餐)
例如,對食物有強烈的執著,嚴謹,了解
當飲食不是只為了將熱量塞到口中,而胡亂進食,對食物有一定認知,己經很難會發胖
我總覺得,想要生活得比較好,減少身體上的問題,出發點 ...
永遠不是少油,永遠不是低脂,永遠不是膽固醇,亦不是鹽的問題
以上種種慨念世界性的全力推行
如果真的因為上面原因,吃少油,低脂,低膽固醇,低鈉的人群,肥胖率,三高率依然節節上昇
現在因為受到健康風氣影響 , French paradox 也開始消失,世界最大問題之一的肥胖,真的就無解嗎
引用 Wiki
Obesity levels in France doubled between 1995 and 2004 (to 11.3% of the population).[3]In 2001 France was reported to have had the lowest obesity rate in Europe
雖然沒有人能証明,但由種種『觀察性資料』所得,離棄了傳統飲食文化,改向速食,改向簡易快捷的食品,情況不樂觀 ..
圖表 :http://www.cbc.ca/…/canada-s-obesity-rate-higher-since-glob…
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