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CGA大戰

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peri

一般的騎士

電梯直達

1^#

發表於 05-2-26 22:05:03 |只看該作者 |降序瀏覽大字中字小字正體化简体化

peri: Kanon的劇場版共有兩集 , 分別為 [ 風花 ] 以及 [ 雪月 ] .
peri: 分享公開的日子是........
?:

peri: ......................

peri : 提早公開實在抱歉啊,我沒想到銀河天使隊是這麼的不受歡迎啊~~!

? :

peri :

< 未完待續 >

Mitochondrial Dysfunction and Type 2 Diabetes

Maintenance of normal blood glucose levels depends on a complex interplay between
the insulin responsiveness of skeletal muscle and liver and glucose-stimulated
insulin secretion by pancreatic b cells. Defects in the former are responsible for insulin

resistance, and defects in the latter are responsible for progression to hyperglycemia.

Emerging evidence supports the potentially unifying hypothesis that both of these

prominent features of type 2 diabetes are caused by mitochondrial dysfunction.

Type 2 diabetes is the most common metabolic disease in the world. In the United States,
it is the leading cause of blindness, end-stage renal disease, and nontraumatic loss of limb,
with associated health care costs estimated to exceed $130 billion per year (1). Of even
greater concern, type 2 diabetes is rapidly becoming a global pandemic and is projected
to afflict more than 300 million individuals worldwide by the year 2025, with most of
the increase occurring in India and Asia (2). Although the primary cause of this disease
unknown, it is clear that insulin resistance plays an early role in its pathogenesis and
that defects in insulin secretion by pancreatic b cells are instrumental in the progression to
hyperglycemia. Here, we explore the potentially unifying hypothesis that these two prominent
features of type 2 diabetes are both attributable to defects in mitochondria, the organelles
that provide energy to the cell.

Role of Intracellular Fatty Acid

Metabolites in Insulin Resistance

Several lines of evidence indicate that insulin resistance is an early feature of type 2
diabetes. First, virtually all patients with type 2 diabetes are insulin-resistant, and prospective
studies have shown that this insulinresistant state develops 1 to 2 decades before
the onset of the disease (3–5). Second, insulin resistance in the offspring of parents
with type 2 diabetes is the best predictor for later development of the disease . Lastly,
perturbations that reduce insulin resistance prevent the development of diabetes .

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play0219

無名的騎士

2^#

發表於 05-2-26 22:18:57 |只看該作者大字中字小字正體化简体化載入全部圖片

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看類型吧~心眼太謎的話最後還是會麻煩到大大身上說QQ"
要在這裡發嗎??那我來搶第一ˊ0ˋ 加入我的最愛當中...
推推推~兔子加油._.a

請至控制面板重新儲存簽名檔

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dryade64752

一般的鄉紳

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發表於 05-2-26 22:46:06 |只看該作者大字中字小字正體化简体化載入全部圖片

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恩~心眼太迷的話真的會很頭痛@@
趕快搶好第2個位子

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lilyrital

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發表於 05-2-26 23:35:44 |只看該作者大字中字小字正體化简体化載入全部圖片

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搶第三
挺難猜的改天問你= ="

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peri

一般的騎士

5^#

發表於 05-2-27 02:23:56 |只看該作者大字中字小字正體化简体化載入全部圖片

回覆: CGA大戰

Skeletal muscle and liver are the two key insulin-responsive organs responsible for maintaining

normal glucose homeostasis, and their transition to an insulin-resistant state accounts

for most of the alterations in glucose metabolism seen in patients with type 2 diabetes.

Before considering whether mitochondrial dysfunction contributes to the development of insulin

resistance in these organs, it is first important to understand the cellular mechanisms responsible

for insulin resistance. As discussed by Lazar , there is growing evidence that circulating

cytokines secreted by fat tissue can modulate the insulin responsiveness of liver

and muscle. However, fatty acids and/or intracellular fatty acid metabolites such as

fatty acyl coenzyme As (fatty acyl CoAs)

, diacylglycerol , or ceramides are also thought to play a critical role.

Over 40 years ago, Randle et al. demonstrated that fatty acids caused insulin resistance

in an in vitro rat muscle preparation, and they hypothesized that this occurred by a

substrate competition mechanism . According to his model, increased oxidation of

muscle fatty acids would produce increased levels of intracellular acetyl CoA and citrate,

which in turn would inhibit, respectively, two enzymes involved in glucose utilization,

pyruvate dehydrogenase and phosphofructokinase.

Inhibition of the glycolytic pathway at these steps would increase intracellular

glucose and glucose-6-phosphate concentrations, ultimately resulting in reduced insulinstimulated

glucose uptake.

More recent studies using 13C and 31P

magnetic resonance spectroscopy (MRS) have

shown that this mechanism for fatty acid–

induced insulin resistance is untenable in human

skeletal muscle ; rather, fatty acids

appear to cause insulin resistance by directly

inhibiting insulin-stimulated glucose transport

activity . This inhibition is likely because

of the accumulation of intracellular

fatty acyl CoAs and diacylglycerol, which then

activate critical signal transduction pathways

that ultimately lead to suppression of insulin

signaling . One might therefore predict

that any metabolic perturbation that promotes

the accumulation of fatty acids in liver

and/or muscle and/or any defect in the ability

of these organs to metabolize fatty acids might

result in insulin resistance . Indeed, defects

in adipocyte metabolism, which occur

in conditions such as severe lipodystrophy

, can result in the former, and it has become

increasingly evident that defects in mitochondrial

fatty acid oxidation can result in the

latter and may be responsible for the more

common forms of insulin resistance.

___________________________________分割線___________________________________

Now here is the question , what's the word of " MRS " ? Please write down the primitive vocabulary in English . --> AIR 的心眼提示!!

Answer : magneticresonancespectroscopy