View source for Insulin resistance/ja

<languages />
{{Infobox medical condition (new)
| name =
| synonyms =
| image =
| caption =
| pronounce =
| field = [[Endocrinology/ja]]
| symptoms =
| complications =
| onset =
| duration =
| types =
| causes =
| risks =
| diagnosis =
| differential =
| prevention =
| treatment =
| medication =
| prognosis =
| frequency =
| deaths =
}}
'''インスリン抵抗性'''（'''IR'''）は、[[cell (biology)/ja|細胞]]がホルモン[[insulin/ja|インスリン]]に正常に反応しないか、または[[hyperinsulinemia/ja|高インスリン血症]]に反応してインスリン受容体の[[downregulation/ja|制御低下]]が起こる[[pathological/ja|病理学的]]状態である。

インスリンは、血液中のブドウ糖を細胞内に運びやすくし、血液中の[[glucose/ja|グルコース]]（血糖値）を下げるホルモンである。インスリンは食事で摂取した炭水化物に反応して[[pancreas/ja|膵臓]]から分泌される。インスリン抵抗性の状態では、同じ量のインスリンでもグルコース輸送と血糖値に対する効果は同じではない。インスリン抵抗性には多くの原因があり、その根本的なプロセスはまだ完全には解明されていない。インスリン抵抗性の危険因子には、[[obesity/ja|肥満]]、[[sedentary lifestyle/ja|座りがちなライフスタイル]]、糖尿病の家族歴、様々な健康状態、特定の医薬品などがある。インスリン抵抗性は[[metabolic syndrome/ja|メタボリックシンドローム]]の構成要素と考えられている。空腹時インスリン値やブドウ糖負荷試験など、インスリン抵抗性を測定する方法は複数あるが、臨床ではあまり用いられない。インスリン抵抗性は、減量、運動、食事の変更などのライフスタイルのアプローチによって改善または逆転させることができる。

==原因==
{{Anchor|Cause}}
===危険因子===
インスリン抵抗性の危険因子には、過体重や肥満、[[sedentary lifestyle/ja|座りがちなライフスタイル]]などがある。また、[[polycystic ovary syndrome/ja|多嚢胞性卵巣症候群]]など、インスリン抵抗性と関連する特定の医学的状態もある。

米国[[:en:National Institute of Diabetes and Digestive and Kidney Diseases|国立糖尿病・消化器・腎臓病研究所]]は、インスリン抵抗性の素因となりうる特定のリスクには以下のようなものがあるとしている：
* 45歳以上である。
* アフリカ系アメリカ人、アラスカ先住民、アメリカン・インディアン、アジア系アメリカ人、ヒスパニック／ラテン系アメリカ人、ネイティブ・ハワイアン、または太平洋諸島系アメリカ人である。
* 高血圧やコレステロール値異常などの健康状態にある。
* 妊娠糖尿病の既往がある。
* 心臓病や脳卒中の既往歴がある。

さらに、医薬品やその他の健康状態によっては、リスクが高まることもある。

===生活習慣要因===
インスリン抵抗性には食事要因が関与していると考えられる。しかし、栄養学的研究の限界を考えると、原因となる食品を特定することは困難である。独自にインスリン抵抗性と関連している食品としては、糖分が多く[[glycemic index/ja|血糖指数]]が高いもの、オメガ3や食物繊維が少ないもの、過食のリスクを高める[[hyperpalatable/ja|過食性]]のものなどがある。脂肪や糖分の多い食事や飲料の過剰摂取は、[[metabolic syndrome/ja|メタボリックシンドローム]]流行の根本的な要因として提唱されている。

食事はまた、細胞膜のリン脂質の多価不飽和脂肪酸と[[saturated fats/ja|飽和脂肪酸]]の比率を変える可能性がある。[[polyunsaturated fatty acids/ja|多価不飽和脂肪酸]]（PUFA）の割合は、インスリン抵抗性と逆相関している。PUFA濃度を高めることによって細胞膜の流動性を高めると、インスリン受容体の数が増加し、インスリンと受容体との親和性が高まり、インスリン抵抗性が低下するという仮説が立てられている。

[[vitamin D/ja|ビタミンD]]の欠乏もインスリン抵抗性と関連している。

座りがちな生活習慣は、インスリン抵抗性発症の可能性を高める。疫学研究では、より高いレベルの身体活動（1日90分以上）は糖尿病のリスクを28％減少させる。

研究では一貫して、インスリン抵抗性と概日リズムには関連があり、インスリン感受性は朝が高く、夕方が低いことが示されている。[[circadian rhythm disorder/ja|概日リズム障害]]のように、[[circadian rhythm/ja|概日リズム]]と食事スケジュールの不一致は、インスリン抵抗性を高める可能性がある。

===医薬品===
[[corticosteroid/ja|コルチコステロイド]]、[[protease inhibitors/ja|プロテアーゼ阻害薬]]（HIV治療薬の一種）、[[atypical antipsychotic/ja|非定型抗精神病薬]]など、いくつかの医薬品はインスリン抵抗性と関連している。

===睡眠中に光を浴びること=== 
睡眠中に光を浴びることは、インスリン抵抗性を引き起こし、心拍数を増加させることが示されている。

===ホルモン===
[[cortisol/ja|コルチゾール]]、[[growth hormone/ja|成長ホルモン]]、[[human placental lactogen/ja|ヒト胎盤性ラクトゲン]]など、多くのホルモンがインスリン抵抗性を誘発する。

コルチゾールは[[insulin/ja|インスリン]]に対抗し、肝[[gluconeogenesis/ja|糖新生]]の亢進、末梢でのグルコース利用の低下、インスリン抵抗性の亢進を引き起こす。これは、[[glucose transporter/ja|グルコーストランスポーター]]（特に[[GLUT4/ja|GLUT4]]）の細胞膜へのトランスロケーションを減少させることによって行われる。

[[bariatric surgery/ja|肥満手術]]後のヒトや十二指腸を外科的に切除したラットにおけるインスリン感受性の有意な改善に基づいて、小腸の初期部分の[[mucosa/ja|粘膜]]で何らかの物質が産生され、体細胞がインスリン抵抗性になるようにシグナルを送っていると提唱されている。産生される組織が除去されれば、シグナルは止まり、体細胞は正常なインスリン感受性に戻る。そのような物質はまだ見つかっておらず、そのような物質の存在は推測の域を出ていない。

[[Leptin/ja|レプチン]]は、ob遺伝子と脂肪細胞から産生されるホルモンである。その生理的役割は、満腹時に身体に警告を発して空腹感を調節することである。

===疾患===
[[PCOS/ja|多嚢胞性卵巣症候群]]や[[NAFLD/ja|非アルコール性脂肪性肝疾患（NAFLD）]]はインスリン抵抗性と関連している。また、[[Hepatitis C/ja|C型肝炎]]は2型糖尿病やインスリン抵抗性を3～4倍発症しやすくする。

<div lang="en" dir="ltr" class="mw-content-ltr">
=== Mitochondrial dysfunction ===
Multiple studies involving different methodology suggest that impaired function of [[Mitochondrion|mitochondria]] might play a pivotal role in the pathogenesis of insulin resistance. Mitochondrial dysfunction may result from the formation of [[reactive oxygen species]], genetic factors, aging, and reduced mitochondrial biogenesis. If confirmed by rigorous studies, a link between mitochondrial disorders and reduced insulin sensitivity might pave the way to new therapeutic approaches.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
=== Inflammation ===
Acute or chronic inflammation, such as in infections, can cause insulin resistance. [[tumor necrosis factor-alpha|TNF-α]] is a cytokine that may promote insulin resistance by promoting [[lipolysis]], disrupting insulin signaling, and reducing the expression of GLUT4.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
=== Genetics ===
Several genetic loci have been determined to be associated with insulin insensitivity. This includes variation in loci near the NAT2, GCKR, and IGFI genes associated with insulin resistance. Further research has shown that loci near the genes are linked to insulin resistance. However, these loci are estimated to account for only 25–44% of the genetic component of insulin resistance.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
==Pathophysiology==
In normal metabolism, the elevated blood glucose instructs beta (β) cells in the [[Islets of Langerhans]], located in the [[pancreas]], to release insulin into the blood. The insulin makes insulin-sensitive tissues in the body (primarily skeletal [[muscle]] cells, [[adipose]] tissue, and [[liver]]) absorb [[glucose]] which provides energy as well as lowers blood glucose. The beta cells reduce insulin output as the blood glucose level falls, allowing blood glucose to settle at a constant of approximately 5&nbsp;mmol/L (90&nbsp;mg/dL). In an ''insulin-resistant'' person, normal levels of insulin do not have the same effect in controlling blood glucose levels.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
When the body produces insulin under conditions of insulin resistance, the cells are unable to absorb or use it as effectively and it stays in the bloodstream. Certain cell types such as [[fat]] and [[muscle]] cells require insulin to absorb glucose and when these cells fail to respond adequately to circulating insulin, blood glucose levels rise. The [[liver]] normally helps regulate glucose levels by reducing its secretion of glucose in the presence of insulin. However, in insulin resistance, this normal reduction in the liver's glucose production may not occur, further contributing to elevated blood glucose.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Insulin resistance in [[adipose tissue|fat cells]] results in reduced uptake of circulating lipids and increased [[hydrolysis]] of stored [[triglyceride]]s. This leads to elevated free [[fatty acid]]s in the [[blood plasma]] and can further worsen insulin resistance. Since insulin is the primary hormonal signal for energy storage into [[fat cells]], which tend to retain their sensitivity in the face of hepatic and skeletal muscle resistance, insulin resistance stimulates the formation of new fatty tissue and accelerates weight gain.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
In states of insulin resistance, [[beta cell]]s in the [[pancreas]] increase their production of insulin. This causes [[hyperinsulinemia|high blood insulin]] (hyperinsulinemia) to compensate for the high blood glucose. During this compensated phase of insulin resistance, [[Pancreatic beta cell function|beta cell function]] is upregulated, insulin levels are higher, and blood glucose levels are still maintained. If compensatory insulin secretion fails, then either fasting (impaired fasting glucose) or postprandial (impaired glucose tolerance) glucose concentrations increase. Eventually, type 2 diabetes occurs when glucose levels become higher as the resistance increases and compensatory insulin secretion fails. The inability of the β-cells to produce sufficient insulin in a condition of hyperglycemia is what characterizes the transition from insulin resistance to type 2 diabetes.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Insulin resistance is strongly associated with intestinal-derived [[Apolipoprotein B|apoB-48]] production rate in insulin-resistant subjects and type 2 diabetics. Insulin resistance often is found in people with visceral adiposity, hypertension, hyperglycemia, and [[dyslipidemia]] involving elevated triglycerides, small dense [[low-density lipoprotein]] (sdLDL) particles, and decreased [[high-density lipoprotein]] (HDL) cholesterol levels. With respect to visceral adiposity, a great deal of evidence suggests two strong links with insulin resistance. First, unlike subcutaneous adipose tissue, visceral adipose cells produce significant amounts of proinflammatory [[cytokines]] such as tumor necrosis factor-alpha ([[TNF-a]]), and [[Interleukins]]-1 and −6, etc. In numerous experimental models, these proinflammatory cytokines disrupt normal insulin action in fat and muscle cells and may be a major factor in causing the whole-body insulin resistance observed in patients with visceral adiposity. Much of the attention on production of proinflammatory cytokines has focused on the IKK-beta/[[NF-kappa-B]] pathway, a protein network that enhances transcription of inflammatory markers and mediators that may cause insulin resistance. Second, visceral adiposity is related to an accumulation of fat in the liver, a condition known as [[non-alcoholic fatty liver disease]] (NAFLD). The result of NAFLD is an excessive release of free fatty acids into the bloodstream (due to increased lipolysis), and an increase in hepatic breakdown of glycogen stores into glucose ([[glycogenolysis]]), both of which have the effect of exacerbating peripheral insulin resistance and increasing the likelihood of [[T2DM|Type 2 diabetes mellitus]].
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
The excessive expansion of adipose tissue that tends to occur under sustainedly positive energy balance (as in overeating) has been postulated by [[Antonio Vidal-Puig|Vidal-Puig]] to induce lipotoxic and inflammatory effects that may contribute to causing insulin resistance and its accompanying disease states.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Also, insulin resistance often is associated with a [[hypercoagulable state]] (impaired [[fibrinolysis]]) and increased inflammatory cytokine levels.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
=== Molecular mechanism ===
At the molecular level, a cell senses insulin through insulin receptors, with the signal propagating through a signaling cascade collectively known as [[PI3K/AKT/mTOR pathway|PI3K/Akt/mTOR signaling pathway]]. Recent studies suggested that the pathway may operate as a [[Bistability#In biological and chemical systems|bistable]] switch under physiologic conditions for certain types of cells, and insulin response may well be a threshold phenomenon. The pathway's sensitivity to insulin may be blunted by many factors such as lipolysis of free fatty acids, causing insulin resistance. From a broader perspective, however, sensitivity tuning (including sensitivity reduction) is a common practice for an organism to adapt to the changing environment or metabolic conditions. Pregnancy, for example, is a prominent change of metabolic conditions, under which the mother has to reduce her muscles' insulin sensitivity to spare more glucose for the brains (the mother's brain and the fetal brain). This can be achieved through raising the response threshold (i.e., postponing the onset of sensitivity) by secreting placental growth factor to interfere with the interaction between insulin receptor substrate (IRS) and PI3K, which is the essence of the so-called ''adjustable threshold hypothesis'' of insulin resistance.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Insulin resistance has been proposed to be a reaction to excess nutrition by [[superoxide dismutase]] in cell [[mitochondria]] that acts as an antioxidant defense mechanism. This link seems to exist under diverse causes of insulin resistance. It also is based on the finding that insulin resistance may be reversed rapidly by exposing cells to mitochondrial uncouplers, [[electron transport chain]] inhibitors, or mitochondrial [[superoxide dismutase mimetics]].
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
==Diagnosis==
===Fasting insulin levels===
A fasting serum insulin level greater than 29 microIU/mL or 174 pmol/L indicates insulin resistance. The same levels apply three hours after the last meal.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
===Glucose tolerance testing===
During a [[glucose tolerance test]] (GTT), which may be used to diagnose diabetes mellitus, a fasting patient takes a 75&nbsp;gram oral dose of glucose. Then blood glucose levels are measured over the following two hours.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Interpretation is based on [[WHO]] guidelines. After two hours a [[blood sugar|glycemia]] less than 7.8&nbsp;mmol/L (140&nbsp;mg/dL) is considered normal, a glycemia of between 7.8 and 11.0&nbsp;mmol/L (140 to 197&nbsp;mg/dL) is considered as [[impaired glucose tolerance]] (IGT), and a glycemia of greater than or equal to 11.1&nbsp;mmol/L (200&nbsp;mg/dL) is considered [[diabetes mellitus]].
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
An [[oral glucose tolerance test]] (OGTT) may be normal or mildly abnormal in simple insulin resistance. Often, there are raised glucose levels in the early measurements, reflecting the loss of a postprandial peak (after the meal) in insulin production. Extension of the testing (for several more hours) may reveal a [[hypoglycemia|hypoglycemic]] "dip," that is a result of an overshoot in insulin production after the failure of the physiologic postprandial insulin response.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
===Hyperinsulinemic euglycemic clamp===
The [[gold standard (test)|gold standard]] for investigating and quantifying insulin resistance is the "hyperinsulinemic euglycemic clamp," so-called because it measures the amount of [[glucose]] necessary to compensate for an increased [[insulin]] level without causing [[hypoglycemia]]. It is a type of [[glucose clamp technique]]. The test is rarely performed in clinical care, but is used in medical research, for example, to assess the effects of different medications. The rate of glucose infusion commonly is referred to in diabetes literature as the GINF value.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
The procedure takes about two hours. Through a [[peripheral vein]], [[insulin]] is infused at 10–120 mU per m<sup>2</sup> per [[minute]]. In order to compensate for the insulin [[intravenous|infusion]], [[glucose]] 20% is infused to maintain blood sugar levels between 5 and 5.5&nbsp;mmol/L. The rate of glucose infusion is determined by checking the [[blood sugar]] levels every five to ten minutes.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
The rate of glucose infusion during the last thirty minutes of the test determines insulin sensitivity. If high levels (7.5&nbsp;mg/min or higher) are required, the patient is insulin-sensitive. Very low levels (4.0&nbsp;mg/min or lower) indicate that the body is resistant to insulin action. Levels between 4.0 and 7.5&nbsp;mg/min are not definitive, and suggest "impaired glucose tolerance," an early sign of insulin resistance.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
This basic technique may be enhanced significantly by the use of glucose tracers. Glucose may be labeled with either stable or radioactive atoms. Commonly used tracers are 3-<sup>3</sup>H glucose (radioactive), 6,6 <sup>2</sup>H-glucose (stable) and 1-<sup>13</sup>C Glucose (stable). Prior to beginning the hyperinsulinemic period, a 3h tracer infusion enables one to determine the basal rate of glucose production. During the clamp, the plasma tracer concentrations enable the calculation of whole-body insulin-stimulated glucose metabolism, as well as the production of glucose by the body (i.e., endogenous glucose production).
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
===Modified insulin suppression test===
Another measure of insulin resistance is the modified insulin suppression test developed by [[Gerald Reaven]] at Stanford University. The test correlates well with the euglycemic clamp, with less operator-dependent error. This test has been used to advance the large body of research relating to the metabolic syndrome.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Patients initially receive 25 μg of [[octreotide]] (Sandostatin) in 5 mL of normal saline over 3 to 5 minutes via intravenous infusion (IV) as an initial bolus, and then, are infused continuously with an intravenous infusion of [[somatostatin]] (0.27 μg/m<sup>2</sup>/min) to suppress endogenous insulin and glucose secretion. Next, insulin and 20% glucose are infused at rates of 32 and 267&nbsp;mg/m<sup>2</sup>/min, respectively. Blood glucose is checked at zero, 30, 60, 90, and 120 minutes, and thereafter, every 10 minutes for the last half-hour of the test. These last four values are averaged to determine the steady-state plasma glucose level (SSPG). Subjects with an SSPG greater than 150&nbsp;mg/dL are considered to be insulin-resistant.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
===Alternatives===
Given the complicated nature of the "clamp" technique (and the potential dangers of [[hypoglycemia]] in some patients), alternatives have been sought to simplify the measurement of insulin resistance. The first was the [[homeostatic model assessment|Homeostatic Model Assessment]] (HOMA), and more recent methods include the [[Quantitative insulin sensitivity check index]] (QUICKI) and [[SPINA-GR]], a measure for insulin sensitivity. All of these calculated markers employ [[fasting]] [[insulin]] and [[glucose]] levels to calculate insulin resistance, and all correlate reasonably with the results of clamping studies.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
==Prevention and management==
Maintaining a healthy body weight and being physically active can help reduce the risk of developing insulin resistance.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
The primary treatment for insulin resistance is [[exercise]] and [[weight loss]]. Both [[metformin]] and [[thiazolidinedione]]s improve insulin sensitivity. Metformin is approved for prediabetes and type 2 diabetes and has become one of the more commonly prescribed medications for insulin resistance.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
The ''Diabetes Prevention Program'' (DPP) showed that exercise and diet were nearly twice as effective as [[metformin]] at reducing the risk of progressing to type 2 diabetes. However, the participants in the DPP trial regained about 40% of the weight that they had lost at the end of 2.8 years, resulting in a similar incidence of diabetes development in both the lifestyle intervention and the control arms of the trial. In epidemiological studies, higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Furthermore, physical training has also generally been seen to be an effective antagonist of insulin resistance in obese or overweight children and adolescents (under the age of 19). As per the 2016 systematic review and meta-analysis conducted by Marson et al., aerobic exercise is associated with fasting insulin reduction; however, resistance and combined exercise are not. The authors caution against demeaning the importance of resistance and combined exercise, as this type of training is generally less researched than aerobic training. Overall, physical training can be used in both adolescents and adults to prevent the progression of insulin resistance and future possible metabolic and cardiovascular disease.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
[[Resistant starch]] from high-amylose corn, [[amylomaize]], has been shown to reduce insulin resistance in healthy individuals, in individuals with insulin resistance, and in individuals with type 2 diabetes.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Some types of [[Polyunsaturated fat|polyunsaturated fatty acids]] ([[omega-3]]) may moderate the progression of insulin resistance into type 2 diabetes, however, omega-3 fatty acids appear to have limited ability to reverse insulin resistance, and they cease to be efficacious once type 2 diabetes is established.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
==History==
The concept that insulin resistance may be the underlying cause of [[diabetes mellitus]] type 2 was first advanced by Professor Wilhelm Falta and published in Vienna in 1931, however, type 2 diabetes does not occur unless there is concurrent failure of compensatory insulin secretion.
</div>

=== 適応的説明 ===
インスリン抵抗性も肥満も、それ自体は代謝異常ではなく、[[lipotoxicity/ja|脂質毒性]]（血流や組織中の脂質の危険なレベル）から臓器を守るための、持続的なカロリー過剰に対する適応反応に過ぎないと主張する学者もいる： 「したがって、肥満は病態や疾患とみなされるべきではなく、むしろ持続的なカロリー過剰に対する正常な生理的反応とみなされるべきである。骨格筋や肝臓を含むインスリン標的組織における高レベルの脂質蓄積の結果として、脂質を多く含む細胞からのグルコースの排除は、脂質生成基質のさらなる蓄積に対する代償的防御であることが示唆されている。"

インスリン抵抗性が進化的適応であるという他の有力な考えには、[[thrifty gene hypothesis/ja|倹約遺伝子仮説]]がある。この仮説は、もしインスリン抵抗性と2型糖尿病に遺伝的要素があるならば、これらの表現型は淘汰されるべきであるというものである。しかし、正常血糖集団においても糖尿病集団においても、平均インスリン抵抗性は増加している。

J.V.ニールは、もともと古代人の祖先が飢饉の多かった時代には、グルコースの貯蔵量を増やすメカニズムを持つ遺伝子が有利だったと仮定している。しかし、現代の環境ではそうではない。

<div lang="en" dir="ltr" class="mw-content-ltr">
Evidence is contradictory to Neel in studies of the Pima Indians, which indicate that the people with higher insulin sensitives tended to weigh the most and conversely people with insulin resistance tended to weigh less on average in this demographic.
</div>

<div lang="en" dir="ltr" class="mw-content-ltr">
Modern hypotheses suggest that insulin metabolism is a socio-ecological adaptation with insulin being the means for differentiating energy allocation to various components of the body and insulin sensitivity an adaptation to manipulate where the energy is diverted to. The Behavioral Switch Hypothesis posits that insulin resistance results in two methods to alter reproductive strategies and behavioral methods. The two strategies are coined as "r to K" and "soldier to diplomat." The r to K strategy involves diverting insulin via placenta to the fetus. This has demonstrated weight gain in the fetus, but not the mother indicating a method of increased parental investment (K strategy). In the "soldier to diplomat" the insensitivity of skeletal muscle to insulin could divert the glucose to the brain, which does not require insulin receptors. This has shown increases in cognitive development across various studies.
</div>

== こちらも参照 ==
{{col div|colwidth=40em}}
* [[Pancreatic beta cell function/ja]]
* [[Chronic Somogyi rebound/ja]]
* [[Hyperinsulinemia/ja]]
* [[Resistin/ja]]
* [[Chronic stress/ja]]
* [[Inflammation/ja#Interleukins and obesity|全身性炎症]]
* [[Circadian rhythm/ja#Obesity and diabetes|概日リズムの乱れ]]
* [[Advanced glycation end-products/ja]]
* [[Polycystic ovary syndrome/ja]]
{{colend}}

== さらに読む ==
{{refbegin}}
* {{cite journal | vauthors = Reaven GM | title = The insulin resistance syndrome: definition and dietary approaches to treatment | journal = Annual Review of Nutrition | volume = 25 | pages = 391–406 | year = 2005 | pmid = 16011472 | doi = 10.1146/annurev.nutr.24.012003.132155 | s2cid = 24849146 | type = review }}
* {{cite journal | vauthors = Rao G | title = Insulin resistance syndrome | journal = American Family Physician | volume = 63 | issue = 6 | pages = 1159–63, 1165–6 | date = March 2001 | pmid = 11277552 | url = http://www.aafp.org/afp/2001/0315/p1159.html | type = review | place = US }}
{{refend}}

== 外部リンク ==
{{Medical resources
| DiseasesDB =
| ICD10 =
| ICD9 =
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj = med
| eMedicineTopic = 1173
}}
* {{Curlie|Health/Conditions_and_Diseases/Endocrine_Disorders/Pancreas/Insulin_Resistance/}}
* {{Cite book | url = http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/ | title = Diabetes | contribution = Insulin resistance | publisher = NIH | location = US | access-date = 2013-04-25 | archive-date = 2015-05-13 | archive-url = https://web.archive.org/web/20150513011234/http://diabetes.niddk.nih.gov/DM/pubs/insulinresistance/ | url-status = dead }}

{{diabetes/ja}}
{{Disease of the pancreas and glucose metabolism/ja}}

{{DEFAULTSORT:Insulin Resistance}}
[[Category:Diabetes]]