Insulin Tolerance(인슐린 내성)란 무엇입니까?
Insulin Tolerance 인슐린 내성 - Body mass, fast blood glucose, and glucose and insulin tolerance were evaluated. [1] Changes in fasting plasma glucose levels, fasting serum insulin levels, glucose and insulin tolerance, glycolipid metabolism, gut microbiota composition (16S rRNA gene sequencing), inflammatory responses, and autophagy in the liver were evaluated. [2] Insulin tolerance was measured at thermoneutrality and after stimulation with cold or the administration of the β3-adrenergic receptor (β3-AR) agonist CL316,243. [3] When fed to HC rats, only diets containing the grilled and boiled shrimp powders significantly prevented the weight loss, lowered fasting and glucose levels, improved glucose and insulin tolerance, and prevented the increase in serum liver markers, ALT and AST. [4] Mice treated with P3DEX also demonstrated improvements in glucose homeostasis and insulin tolerance. [5] Endpoint parameters included bone architecture, structural and estimated tissue-level mechanical properties, body weight/composition, glucose-stimulated insulin secretion, glucose tolerance, insulin tolerance, and metabolic cage analysis. [6] Methods: The glucose and insulin tolerance of diabetic rats were monitored. [7] Endogenous EPO maintains glucose and insulin tolerance and protects against fat mass accumulation and inflammation. [8] While having no effect on body weight regardless of sex, diet, and age, Rap1 deficiency in the VMH SF1 neurons markedly lowered blood glucose and insulin levels, improved glucose and insulin tolerance, and protected mice against HFD-induced neural leptin resistance and peripheral insulin resistance at the cellular and whole-body levels. [9] Results: AG increased fasting levels of glucose and insulin resistance, increased hepatic glucose production, and impaired glucose and insulin tolerance. [10] Results Liver-targeted AAV8-GREM1 did not alter body weight, whole-body glucose and insulin tolerance, or adipose tissue gene expression. [11] FMD cycles increase cardiac vascularity and function and resistance to cardiotoxins, prevent HFCD-dependent hyperglycaemia, hypercholesterolaemia and hyperleptinaemia and ameliorate impaired glucose and insulin tolerance. [12] NBP ameliorated the diabetic state by decreasing glucose levels and improving glucose and insulin tolerance. [13] Glucose tolerance, insulin tolerance, blood glucose and blood lipid levels were measured. [14] Adipose-specific Arx knockout mice have lesser visceral fat and will be used to study the role of Arx in insulin tolerance and obesity. [15] Body and organ weight and parameters of glucose and insulin tolerance were analyzed. [16] RER and EE during cold (10˚C, 72 h), and glucose and insulin tolerance, were not different compared to within-sex WT controls. [17] The health effects of κ-CGN on C57BL/6 J mice were assessed over a 90-d period by monitoring changes in body weight, glucose tolerance, insulin tolerance, fasting glucose and insulin levels, and expression of insulin-pathway-related proteins. [18] The goal of this study was to determine the impact of lipopolysaccharide (LPS)-induced inflammation on changes in glucose and insulin tolerance, performance enhancement, levels of urinary neopterin and concentrations of neurotransmitters in the striatum in mouse models. [19]체질량, 빠른 혈당, 포도당 및 인슐린 내성을 평가했습니다. [1] 공복 혈장 포도당 수치, 공복 혈청 인슐린 수치, 포도당 및 인슐린 내성, 당지질 대사, 장내 미생물 조성(16S rRNA 유전자 염기서열 분석), 염증 반응 및 간에서의 자가포식의 변화를 평가했습니다. [2] 인슐린 내성은 열중성 상태에서 그리고 냉찜질 또는 β3-아드레날린 수용체(β3-AR) 작용제 CL316,243 투여 후 측정되었습니다. [3] HC 쥐에게 구운 새우 분말과 삶은 새우 분말을 함유한 식단만이 체중 감소를 유의하게 예방하고, 공복 및 포도당 수치를 낮추고, 포도당 및 인슐린 내성을 개선하고, 혈청 간 표지자, ALT 및 AST의 증가를 예방했습니다. [4] P3DEX로 치료한 마우스는 또한 포도당 항상성과 인슐린 내성이 개선되었음을 보여주었습니다. [5] 종점 매개변수에는 뼈 구조, 구조적 및 추정된 조직 수준 기계적 특성, 체중/구성, 포도당 자극 인슐린 분비, 포도당 내성, 인슐린 내성 및 대사 케이지 분석이 포함되었습니다. [6] 방법: 당뇨병 쥐의 포도당과 인슐린 내성을 관찰하였다. [7] 내인성 EPO는 포도당 및 인슐린 내성을 유지하고 지방량 축적 및 염증으로부터 보호합니다. [8] 성별, 식이 및 연령에 관계없이 체중에 영향을 미치지 않는 반면 VMH SF1 뉴런의 Rap1 결핍은 혈당 및 인슐린 수치를 현저히 낮추고 포도당 및 인슐린 내성을 개선하며 HFD 유발 신경 렙틴 내성 및 말초 인슐린으로부터 마우스를 보호합니다 세포 및 전신 수준의 저항. [9] 결과: AG는 공복시 포도당 수준과 인슐린 저항성을 증가시켰고, 간 포도당 생산을 증가시켰고, 포도당과 인슐린 내성을 손상시켰습니다. [10] 결과 간 표적 AAV8-GREM1은 체중, 전신 포도당 및 인슐린 내성 또는 지방 조직 유전자 발현을 변경하지 않았습니다. [11] FMD 주기는 심장 혈관과 기능 및 심장 독소에 대한 내성을 증가시키고 HFCD 의존성 고혈당증, 고콜레스테롤혈증 및 고렙틴혈증을 예방하고 손상된 포도당 및 인슐린 내성을 개선합니다. [12] NBP는 포도당 수치를 낮추고 포도당과 인슐린 내성을 개선하여 당뇨병 상태를 개선했습니다. [13] 포도당 내성, 인슐린 내성, 혈당 및 혈중 지질 수치를 측정했습니다. [14] Adipose-specific Arx 녹아웃 마우스는 내장 지방이 적고 인슐린 내성과 비만에서 Arx의 역할을 연구하는 데 사용될 것입니다. [15] 신체 및 장기 무게와 포도당 및 인슐린 내성의 매개변수를 분석했습니다. [16] 추위(10˚C, 72시간) 동안의 RER 및 EE, 그리고 포도당 및 인슐린 내성은 성별 내 WT 대조군과 다르지 않았습니다. [17] C57BL/6 J 마우스에 대한 κ-CGN의 건강 효과는 체중, 포도당 내성, 인슐린 내성, 공복 혈당 및 인슐린 수치, 인슐린 경로 관련 단백질 발현의 변화를 모니터링하여 90일 동안 평가되었습니다. [18] 이 연구의 목표는 마우스 모델의 선조체에서 포도당 및 인슐린 내성, 성능 향상, 요중 네오프테린 수준 및 신경 전달 물질 농도의 변화에 대한 지질다당류(LPS) 유도 염증의 영향을 결정하는 것이었습니다. [19]
oral glucose tolerance 경구 포도당 내성
Insulin tolerance was impaired, but the oral glucose tolerance was improved through an increase in GLP-1 secretion. [1] Preoperative oral glucose tolerance test (OGTT), insulin tolerance test (ITT), and mixed meal tolerance test (MMTT) were repeated at designated time points postoperatively. [2] Our results showed that the ginsenoside Ro (90mg/kg) treatment ameliorated body weight and lipid accumulation in multiple metabolic organs of high-fat diet–induced obese (DIO) mice without affecting food intake and improved oral glucose tolerance tests, intraperitoneal insulin tolerance tests, and fasting serum glucose. [3] Afterward, blood glucose, insulin, and glycogen content were assayed, and insulin tolerance test (ITT), oral glucose tolerance test (OGTT) were performed. [4] At day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. [5] Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT) were used to assess pre-diabetic status. [6] Oral glucose tolerance test (OGTT) and Insulin Tolerance Test (ITT) were performed to determine the extent of insulin resistance in HFD fed male Wistar rats. [7] Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were also performed. [8] Oral glucose tolerance test (OGTT), insulin tolerance test (ITT), fasting blood glucose (FBG), total cholesterol (TC) and triglyceride (TG) were used to assay the disorder of glycolipid metabolism. [9] Hence, we subjected NPGL-precursor gene (Npgl)-overexpressing mice to the oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) under normal chow (NC) and HFD conditions. [10] The groups were monitored for weight, oral glucose tolerance, insulin tolerance, bioavailability, biochemical parameters, and histopathological studies. [11] An oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were also performed in obese diabetic mice. [12] Oral glucose tolerance tests showed that Npgl overexpression maintained glucose tolerance and increased blood insulin levels, and intraperitoneal insulin tolerance tests showed that it maintained insulin sensitivity. [13] The blood glucose levels, oral glucose tolerance test, insulin tolerance test, HOMA-IR for insulin resistance, serum biochemical parameters, and the histopathological changes of adipose tissue, liver and other organs were detected at designed time point. [14] Periodontal indices (plaque index, gingival bleeding index, pocket depth, and clinical attachment loss), insulin sensitivity using the Short Insulin Tolerance Test index (KITT), glucose tolerance derived from oral glucose tolerance test, and serum CRP level were measured before and 3 months after the intervention. [15] Oral glucose tolerance and insulin tolerance were ameliorated by the peptide treatment. [16] Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were performed to assess the anti-diabetic effects of LXT34 in db/db mice, and chronic inflammation in liver and adipose tissues were investigated using histomorphology, immunoblot and gene expression analysis. [17] Computed tomography, indirect calorimetry, and histological analyses including electron microscopy of the liver were performed, and biochemical profiles and oral glucose tolerance test and insulin tolerance test were undertaken. [18] SL sedentary group showed increased body weight, adiposity, and decreased relative weight of the seminal vesicle, prostate, and epididymis as well as changes in the insulin tolerance and oral glucose tolerance tests glycemic tests compared to CL sedentary group. [19] Blood glucose, oral glucose tolerance test, insulin tolerance test, pancreatic histopathology and serum biochemistry were detected to assess the hypoglycemic effect of HDB. [20] Oral glucose tolerance tests showed that Npgl overexpression maintained glucose tolerance and increased blood insulin levels, and intraperitoneal insulin tolerance tests showed that it maintained insulin sensitivity. [21] Oral glucose tolerance and insulin tolerance tests were used to assess insulin sensitivity. [22] Insulin sensitivity and glucose tolerance were evaluated using the insulin tolerance test (ITT) and oral glucose tolerance test (OGTT). [23] Following the behavior test, insulin tolerance test, oral glucose tolerance test (OGTT) and intraperitoneal glucose tolerance test (IPGTT) were performed. [24] RESULTS MBSJ improved the oral glucose tolerance and insulin tolerance, and reduced fasting blood glucose, glycosylated hemoglobin, total cholesterol, triglyceride, and low-density lipoprotein levels in the serum of diabetic rats. [25] Oral glucose tolerance and insulin tolerance tests were performed in week 15 and 17, respectively. [26] Oral glucose tolerance test and insulin tolerance test, obesity and histological examination, serum cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity in high-fat diet-fed rats were analyzed. [27] Oral glucose tolerance test and insulin tolerance test were performed before and 8 weeks after surgery. [28] Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were conducted immediately after FGF21 injection. [29] Interestingly, despite secreting less insulin, KDM5B-KO mice were able to maintain normoglycemia following oral glucose tolerance test, likely via improved insulin sensitivity, as suggested by insulin tolerance testing and phosphorylation of proteins belonging to the insulin signaling pathway. [30]인슐린 내성은 손상되었지만 GLP-1 분비의 증가를 통해 경구 포도당 내성이 개선되었습니다. [1] 수술 전 경구 포도당 내성 검사(OGTT), 인슐린 내성 검사(ITT) 및 혼합 식사 내성 검사(MMTT)는 수술 후 지정된 시점에서 반복되었습니다. [2] 우리의 결과는 ginsenoside Ro(90mg/kg) 치료가 음식 섭취에 영향을 미치지 않고 고지방식이 유도 비만(DIO) 마우스의 여러 대사 기관에서 체중 및 지질 축적을 개선하고 경구 내당능 시험, 복강 내 인슐린 내성 시험을 개선하는 것으로 나타났습니다. , 및 공복 혈청 글루코스. [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] nan [14] 치주 지수(플라그 지수, 치은 출혈 지수, 포켓 깊이, 임상 부착 손실), KITT(Short Insulin Tolerance Test) 지수를 이용한 인슐린 감수성, 경구 내당능 검사에서 파생된 내당능, 혈청 CRP 수치를 측정하기 전과 3 개입 후 몇 달. [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23] nan [24] nan [25] nan [26] nan [27] nan [28] nan [29] nan [30]
glucose tolerance test 포도당 내성 검사
Glucose tolerance tests and insulin tolerance tests were employed to assess insulin resistance. [1] 30 days later, glucose tolerance test (GTT) and insulin tolerance test (ITT) were performed. [2] Series of blood samples were collected for 6 h pulsatile GH profile, glucose tolerance test and insulin tolerance test at 5, 8, and 9 weeks of TRF, respectively. [3] Sunitinib led to the decreased insulin sensitivity as determined by insulin tolerance test (ITT) and glucose tolerance test (GTT), reflecting insulin resistance occurred in sunitinib-treated rats. [4] Results It was found that glucose tolerance test (GTT), insulin tolerance test (ITT), TG, and TC indicated lower levels in the serum of NAFLD/T2DM mice receiving 4 pmol/g and 12 pmol/g metabolitin compared to the mice receiving normal saline (P < 0. [5] The present study demonstrates that the effects of chemerin on adipose tissue is depot different, and specific knock down chemerin in SAT promote adipogenesis and improve glucose tolerance test (GTT) and insulin tolerance test (ITT). [6] Series of blood samples were collected for pulsatile GH analysis, glucose tolerance test (GTT) and insulin tolerance test (ITT) at 9, 10, 11 weeks from the start of intervention, respectively. [7] LCN2 knockout (LCN2KO) mice and wild-type littermates were used to evaluate the effect of LCN2 on insulin sensitivity and hepatic gluconeogenesis through pyruvate tolerance test (PTT), glucose tolerance test (ipGTT), insulin tolerance test (ITT), and hyperinsulinemic-euglycemic clamps, respectively. [8] Glucose tolerance tests (GTT) and insulin tolerance tests (ITT) were performed every 2 weeks. [9] Glucose tolerance test (GTT) and insulin tolerance test (ITT) GTT and ITT were performed, as previously described. [10] Glucose tolerance test (GTT) and insulin tolerance test (ITT) were employed to evaluate the glucose tolerance status. [11] The antidiabetic role of VF5 in HFD fed mice was assessed by glucose tolerance test (GTT) and insulin tolerance test (ITT), fasting plasma insulin level, fasting blood glucose level, AKT signal in peripheral tissue in the absence of toxic effects. [12] 05); the results of glucose tolerance test at 0, 30, 60, 120 min and insulin tolerance test at 0, 30, 60, 90, 120 min in the model group were higher than those in the normal group (P<0. [13] Metabolic analysis was performed by measuring fasted blood glucose and insulin levels and by glucose tolerance test and insulin tolerance test. [14] We show that infusion of the μ‐opioid receptor agonist [d‐Ala2, N‐MePhe4, Gly‐ol]‐enkephalin (DAMGO) in the nucleus accumbens by itself does not affect blood glucose levels, but it enhances the glycaemic response after both an insulin tolerance test, as well as a glucose tolerance test. [15] At 85 days of treatment, an insulin tolerance test (ITT) and glucose tolerance test (GTT) was performed. [16] Further metabolic disorders, such as a lower tolerance to glucose (glucose tolerance test, GTT) and a higher resistance to insulin (insulin tolerance test, ITT) were found in Tg. [17] glucose tolerance tests and overnight fasting-1 h refeeding tests, insulin tolerance by i. [18]인슐린 저항성을 평가하기 위해 포도당 내성 검사와 인슐린 내성 검사가 사용되었습니다. [1] 30일 후 포도당 내성 검사(GTT)와 인슐린 내성 검사(ITT)를 시행하였다. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] nan [14] nan [15] nan [16] nan [17] nan [18]
high fat diet 고지방 다이어트
As a consequence, it reduces body weight and blood glucose levels and improves glucose and insulin tolerance in both ob/ob and high-fat diet-induced obese mouse models. [1] N1+/− mice showed impaired glucose and insulin tolerance with downregulation of IRS-1 and GLUT4 in WAT after high-fat diet. [2] Male mice deficient for PERK in POMC neurons exhibited improvements in energy balance on a high-fat diet, showing decreased food intake and body weight, independent of changes in glucose and insulin tolerances. [3] Glucose and insulin tolerance test (GTT/ITT) were performed on both chow fed or high fat diet (HFD) fed offspring to examine the glucose metabolism status. [4] Forskolin administration linearly decreased blood glucose levels of high-fat diet-fed mice at 90 min and total area under curve (AUC) after insulin tolerance test. [5] Effects of a high-fat diet were analysed by glucose tolerance and insulin tolerance tests. [6] METHODS The GDM model was established in mice by high-fat diet, treated with miR-23a-3p antagomiR, and further performed with glucose and insulin tolerance tests. [7] C57BL/6J mice (WT) and RAGE deficient (RAGE −/− ) mice were fed a high fat diet (HFD) and subjected to glucose and insulin tolerance tests. [8] Adoptive transfer of adiponectin-expressing Treg precursors effectively attenuated obesity, improved glucose and insulin tolerance, prevented fatty liver injuries in wild-type mice fed a high-fat diet, and significantly inhibited breast cancer development in MMTV-PyVT transgenic mice. [9] Feeding rats with high-fat diet (HFD) with a single streptozotocin (STZ) injection induced obesity, slightly elevated fasting blood glucose and impaired glucose and insulin tolerance, and caused cardiac hypertrophy and mild diastolic dysfunction as published before by Koncsos et al. [10] Results: Both male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. [11]결과적으로 ob/ob 및 고지방식이 유도 비만 마우스 모델 모두에서 체중과 혈당 수준을 감소시키고 포도당 및 인슐린 내성을 개선합니다. [1] N1+/- 마우스는 고지방식이 후 WAT에서 IRS-1 및 GLUT4의 하향조절과 함께 손상된 포도당 및 인슐린 내성을 나타냈다. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11]
fasting blood glucose 공복 혈당
Long-term (11-week) consumption of GH tended to reduce body weight and the fasting blood glucose concentration of the HFD-fed mice, and ameliorated glucose intolerance and insulin resistance, according to glucose and insulin tolerance tests. [1] Fasting blood glucose was measured and an insulin tolerance test (ITT) was performed on Day 85 to measure insulin sensitivity and glucose uptake. [2] Fasting blood glucose, fasting serum insulin, the glucose tolerance test (GTT), and the insulin tolerance test (ITT) were measured to evaluate IR of obese mice. [3] Moreover, Danning tablets could improve fasting blood glucose levels and ameliorate glucose and insulin tolerance in HFD-induced obese mice. [4] Traf5−/− mice showed an increased weight gain, impaired insulin tolerance, and increased fasting blood glucose. [5] The levels of fasting blood glucose (FBG) were measured, and the oral glucose tolerance test (OGTT) as well as the insulin tolerance test (ITT) were carried out to assess glycemic status. [6] Metabolic parameters were evaluated by measuring fasting blood glucose, serum insulin, oral glucose and insulin tolerance test. [7] Various doses of SGD were administered, followed by measurements of fasting blood glucose, oral glucose tolerance tests, insulin tolerance tests, markers of lipid metabolism - including free fatty acids (FFA), triglycerides (TG), and total cholesterol (TC) - liver histology, and expression levels of implicated molecules including PI3K/AKT and PPARα. [8] With the rats at 14 weeks of age, we determined the following: (a) fasting blood glucose, (b) oral glucose tolerance, and (c) insulin tolerance. [9]GH의 장기간(11주) 소비는 포도당 및 인슐린 내성 테스트에 따르면 HFD를 섭취한 마우스의 체중과 공복 혈당 농도를 감소시키는 경향이 있었고, 포도당 불내성 및 인슐린 저항성을 개선했습니다. [1] 공복 혈당을 측정하고 85일째 인슐린 내성 검사(ITT)를 수행하여 인슐린 민감도 및 포도당 흡수를 측정했습니다. [2] nan [3] nan [4] Traf5-/- 마우스는 증가된 체중 증가, 손상된 인슐린 내성 및 증가된 공복 혈당을 나타냈다. [5] nan [6] nan [7] nan [8] nan [9]
intraperitoneal glucose tolerance 복강내 포도당 내성
Blood glucose levels were also analyzed using intraperitoneal glucose tolerance and insulin tolerance tests. [1] However, the plasma glucose level at other time points of the IMM group was higher than that of the CON group during an intraperitoneal glucose tolerance test (IPGTT) and an insulin tolerance test (ITT) (p < 0. [2] After male C57BL/6J mice were exposed to arsenite (0 or 20 ppm) in drinking water for 12 months, intraperitoneal glucose tolerance tests (IPGTTs) and insulin tolerance tests (ITTs) revealed an arsenite-induced glucose metabolism disorder. [3] After four weeks of feeding, the insulin tolerance test (ITT), intraperitoneal glucose tolerance test (IPGTT), and HE-clamp study were performed. [4] The intraperitoneal glucose tolerance test and insulin tolerance test showed that ANP treatment significantly ameliorated HFD-induced insulin resistance. [5] At the 6th week of intervention, glucose contents of intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test (IPITT) were measured. [6] Similarly, oral and intraperitoneal glucose tolerance, plasma insulin responses, islet histology, body weight gain, and insulin tolerance were not different in mice with targeted recombination of Tcf7 in insulin-positive β-cells. [7] HFD plus NaCl-fed mice had lower plasma glucose levels in an insulin tolerance test, and showed higher plasma glucose and lower plasma insulin levels in an intraperitoneal glucose tolerance test compared to HFD-fed mice. [8] In the ND group, though the HGF-Tg-ND mice showed higher fasted blood glucose levels and larger integrated density (IOD) of glucagon-positive cells than WT-ND mice, we found that HGF-Tg-ND mice can still maintain normal glucose tolerance based on an intraperitoneal glucose tolerance test (IPGTT) and an intraperitoneal insulin tolerance test (IPITT). [9]혈당 수치는 또한 복강 내 포도당 내성 및 인슐린 내성 테스트를 사용하여 분석되었습니다. [1] 그러나 IMM 그룹의 다른 시점에서의 혈장 포도당 수준은 복강 내 포도당 내성 검사(IPGTT) 및 인슐린 내성 검사(ITT)에서 CON 그룹보다 높았습니다(p < 0. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9]
improved insulin sensitivity 개선된 인슐린 감수성
miR-1-treated mice did not lose weight but had improved insulin sensitivity measured by insulin tolerance test. [1] Prolastin-treated mice fed a HFD had improved insulin sensitivity, as assessed by insulin tolerance test, and this was associated with higher insulin-dependent IRS-1 (insulin receptor substrate) and AktSer473phosphorylation, and reduced inflammation markers in WAT but not liver or muscle. [2] Glucose and insulin tolerance tests showed that ME improved insulin sensitivity. [3] Further, MIP-Cre/ERT;Ghsrf/f mice exhibited improved insulin sensitivity during insulin tolerance tests (ITT). [4]miR-1을 처리한 마우스는 체중이 감소하지 않았지만 인슐린 내성 테스트에 의해 측정된 인슐린 감수성이 개선되었습니다. [1] HFD를 먹인 프롤라스틴 처리 마우스는 인슐린 내성 테스트로 평가한 바와 같이 인슐린 감수성이 개선되었으며, 이는 더 높은 인슐린 의존성 IRS-1(인슐린 수용체 기질) 및 AktSer473인산화와 관련되었으며 WAT의 염증 마커 감소와 관련되었지만 간이나 근육은 그렇지 않았습니다. . [2] nan [3] nan [4]
white adipose tissue 백색 지방 조직
After 12 weeks of HFD, white adipose tissue depots in CPS offspring were increased further, and higher IGTT and lower intraperitoneal insulin tolerance response were found, despite the lack of changes in food intake. [1] Two sublines of rats with high and low whole-body 5HT tone, obtained by selective breeding for platelet 5HT parameters, were examined for fat accumulation in different white adipose tissue (WAT) depots, glucose/insulin tolerance, blood metabolic parameters, and expression of various metabolic genes. [2] ET-1 receptor blockade significantly improved insulin tolerance compared to insulin resistant HFD mice and lowered expression of genes in epididymal white adipose tissue (eWAT) associated with insulin resistance and inflammation. [3]HFD 12주 후, CPS 자손의 백색 지방 조직 저장소가 더 증가하였고, 음식 섭취의 변화가 없음에도 불구하고 더 높은 IGTT 및 더 낮은 복강 내 인슐린 내성 반응이 발견되었습니다. [1] 혈소판 5HT 매개변수에 대한 선택적 번식에 의해 얻은 높고 낮은 전신 5HT 톤을 가진 쥐의 두 하위 계통은 서로 다른 백색 지방 조직(WAT) 저장소에서의 지방 축적, 포도당/인슐린 내성, 혈액 대사 매개변수 및 발현에 대해 조사되었습니다. 다양한 대사 유전자. [2] ET-1 수용체 차단은 인슐린 저항성 HFD 마우스와 비교하여 인슐린 내성을 유의하게 개선하고 인슐린 저항성 및 염증과 관련된 부고환 백색 지방 조직(eWAT)의 유전자 발현을 낮췄습니다. [3]
body weight gain 체중 증가
Prediabetic mice showed mild hyperglycemia, reduced body weight gain, and an increase in glucose and insulin tolerance tests (AUCs). [1] The combination of Arazyme and ESLs significantly suppressed body weight gain, improved glucose and insulin tolerance, and suppressed hepatic steatosis by reducing lipid synthesis and enhancing lipid utilization gene expression. [2]당뇨병 전증 쥐는 경미한 고혈당증, 체중 증가 감소, 포도당 및 인슐린 내성 검사(AUC) 증가를 보였습니다. [1] Arazyme과 ESL의 조합은 지질 합성을 감소시키고 지질 이용 유전자 발현을 향상시켜 체중 증가를 유의하게 억제하고, 포도당 및 인슐린 내성을 개선하고, 간 지방증을 억제했습니다. [2]
body weight body 체중 몸
Empagliflozin did not affect the body weight, body composition or insulin sensitivity (assessed by intraperitoneal insulin tolerance test), but significantly improved glucose homeostasis as assessed by oral glucose tolerance test in DIO-NASH mice. [1] Food intake, body weight, body composition, muscle function, insulin tolerance, and inflammatory status were assessed. [2]엠파글리플로진은 체중, 체성분 또는 인슐린 감수성(복강 내 인슐린 내성 테스트로 평가)에 영향을 미치지 않았지만 DIO-NASH 마우스의 경구 내당능 테스트에서 평가한 바와 같이 혈당 항상성을 유의하게 개선했습니다. [1] 음식 섭취, 체중, 체성분, 근육 기능, 인슐린 내성 및 염증 상태를 평가했습니다. [2]
weight body composition 체중 체성분
We measured weight, body composition, glucose and insulin tolerance, basal metabolism and tibia length and weight in adult mice. [1]우리는 성인 쥐의 체중, 체성분, 포도당 및 인슐린 내성, 기초 대사 및 경골 길이와 체중을 측정했습니다. [1]
Intraperitoneal Insulin Tolerance 복강내 인슐린 내성
Our results showed that the ginsenoside Ro (90mg/kg) treatment ameliorated body weight and lipid accumulation in multiple metabolic organs of high-fat diet–induced obese (DIO) mice without affecting food intake and improved oral glucose tolerance tests, intraperitoneal insulin tolerance tests, and fasting serum glucose. [1] After 12 weeks of HFD, white adipose tissue depots in CPS offspring were increased further, and higher IGTT and lower intraperitoneal insulin tolerance response were found, despite the lack of changes in food intake. [2] Hence, we subjected NPGL-precursor gene (Npgl)-overexpressing mice to the oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) under normal chow (NC) and HFD conditions. [3] Empagliflozin did not affect the body weight, body composition or insulin sensitivity (assessed by intraperitoneal insulin tolerance test), but significantly improved glucose homeostasis as assessed by oral glucose tolerance test in DIO-NASH mice. [4] Oral glucose tolerance tests showed that Npgl overexpression maintained glucose tolerance and increased blood insulin levels, and intraperitoneal insulin tolerance tests showed that it maintained insulin sensitivity. [5] At the 6th week of intervention, glucose contents of intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test (IPITT) were measured. [6] 001), and improved glucose tolerance and insulin sensitivity, as indicated by oral glucose and intraperitoneal insulin tolerance tests. [7] Oral glucose tolerance tests showed that Npgl overexpression maintained glucose tolerance and increased blood insulin levels, and intraperitoneal insulin tolerance tests showed that it maintained insulin sensitivity. [8] Intraperitoneal insulin tolerance testing showed that M-BC and H-BC improved insulin resistance. [9] Intraperitoneal insulin tolerance test (IPITT) was carried out to evaluate the effect of miR-129-5p on IR in NAFLD animal model. [10] In the ND group, though the HGF-Tg-ND mice showed higher fasted blood glucose levels and larger integrated density (IOD) of glucagon-positive cells than WT-ND mice, we found that HGF-Tg-ND mice can still maintain normal glucose tolerance based on an intraperitoneal glucose tolerance test (IPGTT) and an intraperitoneal insulin tolerance test (IPITT). [11] At 8 weeks after injection, intraperitoneal insulin tolerance tests (IPITTs) and insulin release tests (IRTs) were performed. [12]우리의 결과는 ginsenoside Ro(90mg/kg) 치료가 음식 섭취에 영향을 미치지 않고 고지방식이 유도 비만(DIO) 마우스의 여러 대사 기관에서 체중 및 지질 축적을 개선하고 경구 내당능 시험, 복강 내 인슐린 내성 시험을 개선하는 것으로 나타났습니다. , 및 공복 혈청 글루코스. [1] HFD 12주 후, CPS 자손의 백색 지방 조직 저장소가 더 증가하였고, 음식 섭취의 변화가 없음에도 불구하고 더 높은 IGTT 및 더 낮은 복강 내 인슐린 내성 반응이 발견되었습니다. [2] nan [3] 엠파글리플로진은 체중, 체성분 또는 인슐린 감수성(복강 내 인슐린 내성 테스트로 평가)에 영향을 미치지 않았지만 DIO-NASH 마우스의 경구 내당능 테스트에서 평가한 바와 같이 혈당 항상성을 유의하게 개선했습니다. [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12]
Improved Insulin Tolerance 개선된 인슐린 내성
As a result of these effects, in a mouse model of acute hyperuricemia, metformin improved insulin tolerance and glucose tolerance, accompanied by increased AMPK phosphorylation, Akt phosphorylation and translocation of GLUT4 in myocardial tissues. [1] 02) and an improved insulin tolerance (p = 0. [2] At 9 months of age, only male LS12 mice showed improved glucose tolerance and male LS12 mice also showed improved insulin tolerance starting at 5 months of age. [3] Insulin resistance was also markedly ameliorated, as indicated by notably improved insulin tolerance and homeostatic model assessment for insulin resistance (HOMA-IR). [4] ET-1 receptor blockade significantly improved insulin tolerance compared to insulin resistant HFD mice and lowered expression of genes in epididymal white adipose tissue (eWAT) associated with insulin resistance and inflammation. [5] As a result of these effects, in a mouse model of acute hyperuricaemia, metformin improved insulin tolerance and glucose tolerance, accompanied by increased AMPK phosphorylation, Akt phosphorylation and translocation of GLUT4 in myocardial tissues. [6] RESULTS AG-OVXt group increased aerobic performance in 35%, decreased adipose tissue and triglycerides in 36% and 27%, respectively, and improved insulin tolerance in 50% in comparison to AG-OVX. [7]이러한 효과의 결과, 급성 고요산혈증의 마우스 모델에서 메트포르민은 심근 조직에서 AMPK 인산화, Akt 인산화 및 GLUT4 전위 증가와 함께 인슐린 내성과 포도당 내성을 개선했습니다. [1] 02) 및 개선된 인슐린 내성(p = 0. [2] nan [3] nan [4] ET-1 수용체 차단은 인슐린 저항성 HFD 마우스와 비교하여 인슐린 내성을 유의하게 개선하고 인슐린 저항성 및 염증과 관련된 부고환 백색 지방 조직(eWAT)의 유전자 발현을 낮췄습니다. [5] nan [6] nan [7]
Restored Insulin Tolerance 회복된 인슐린 내성
Remarkably, while inhibiting ceramide synthesis exerted no influences on TREM2-dependent ATM remodeling, inflammation, or lipid load, it restored insulin tolerance, reversing adipose hypertrophy and secondary hepatic steatosis of TREM2-deficient animals. [1] Treatment with catalase—a H2O2 dismutase—restored insulin tolerance to WT (wild type) levels in mIGFREO. [2]놀랍게도, 세라마이드 합성을 억제하는 것은 TREM2 의존성 ATM 리모델링, 염증 또는 지질 부하에 영향을 미치지 않았지만, 인슐린 내성을 회복시켜 TREM2 결핍 동물의 지방 비대 및 이차 간 지방증을 역전시켰습니다. [1] H2O2 디스뮤타제인 카탈라아제를 사용한 치료는 mIGFREO에서 WT(야생형) 수준으로 인슐린 내성을 회복했습니다. [2]
Impaired Insulin Tolerance 인슐린 내성 장애
Interestingly, despite the increased energy expenditure, we observed a promotion of adipose tissue inflammation and an ectopic accumulation of triglycerides in the peripheral tissues in Prmt1 adipocyte-specific knockout mice, which promoted the impaired insulin tolerance that is reminiscent of mouse models of lipodystrophy. [1] Traf5−/− mice showed an increased weight gain, impaired insulin tolerance, and increased fasting blood glucose. [2]흥미롭게도, 증가된 에너지 소비에도 불구하고 우리는 지방이영양증의 마우스 모델을 연상시키는 손상된 인슐린 내성을 촉진하는 Prmt1 지방세포 특이적 녹아웃 마우스에서 지방 조직 염증의 촉진과 말초 조직에서 트리글리세리드의 이소성 축적을 관찰했습니다. [1] Traf5-/- 마우스는 증가된 체중 증가, 손상된 인슐린 내성 및 증가된 공복 혈당을 나타냈다. [2]
Short Insulin Tolerance 짧은 인슐린 내성
INTERVENTION(S) Short insulin tolerance test (ITT). [1] Periodontal indices (plaque index, gingival bleeding index, pocket depth, and clinical attachment loss), insulin sensitivity using the Short Insulin Tolerance Test index (KITT), glucose tolerance derived from oral glucose tolerance test, and serum CRP level were measured before and 3 months after the intervention. [2]개입 짧은 인슐린 내성 검사(ITT). [1] 치주 지수(플라그 지수, 치은 출혈 지수, 포켓 깊이, 임상 부착 손실), KITT(Short Insulin Tolerance Test) 지수를 이용한 인슐린 감수성, 경구 내당능 검사에서 파생된 내당능, 혈청 CRP 수치를 측정하기 전과 3 개입 후 몇 달. [2]
insulin tolerance test 인슐린 내성 검사
Serum biochemical parameters were analyzed, and intraperitoneal glucose and insulin tolerance tests were performed. [1] Insulin tolerance tests and glucose tolerance were used to determine progression to insulin resistance and glucose intolerance. [2] Furthermore, a variety of well‐established dynamic tests have been used to diagnose and assess the integrity of the HPA axis, such as the insulin tolerance test, the metyrapone stimulation test and the adrenocorticotropic hormone stimulation test. [3] The insulin sensitivity was assessed by glucose (GTT) and insulin tolerance test (ITT). [4] Blood glucose levels were also analyzed using intraperitoneal glucose tolerance and insulin tolerance tests. [5] Glucose tolerance tests and insulin tolerance tests were employed to assess insulin resistance. [6] The insulin tolerance test (ITT) and HE-clamp were performed after administration of the diets for 4 and 7 weeks. [7] After 30 days of treatment, animals were fasted to perform oral glucose and insulin tolerance test to estimate glucose and insulin levels. [8] miR-1-treated mice did not lose weight but had improved insulin sensitivity measured by insulin tolerance test. [9] Objective: To introduce a relatively convenient and effective way of conducting Insulin Tolerance Test for diagnosis of Growth Hormone deficiency in children with short stature. [10] However, there are no currently reliable data on morning serum cortisol for prediction of cortisol response to insulin tolerance test (ITT). [11] Compared to vehicle control, baricitinib treatment significantly improved insulin resistance examined by insulin tolerance test and increased UCP1 (a key browning marker) expression in perigonadal (pAT) and inguinal AT (iAT), but did not affect weight gain and AT mass. [12] SOD1G93A mice and their wild‐type littermates underwent indirect calorimetry and intraperitoneal glucose/insulin tolerance tests at both the onset and mid‐symptomatic stages of the disease. [13] Preoperative oral glucose tolerance test (OGTT), insulin tolerance test (ITT), and mixed meal tolerance test (MMTT) were repeated at designated time points postoperatively. [14] However, the plasma glucose level at other time points of the IMM group was higher than that of the CON group during an intraperitoneal glucose tolerance test (IPGTT) and an insulin tolerance test (ITT) (p < 0. [15] Long-term (11-week) consumption of GH tended to reduce body weight and the fasting blood glucose concentration of the HFD-fed mice, and ameliorated glucose intolerance and insulin resistance, according to glucose and insulin tolerance tests. [16] Fasting blood glucose was measured and an insulin tolerance test (ITT) was performed on Day 85 to measure insulin sensitivity and glucose uptake. [17] Prediabetic mice showed mild hyperglycemia, reduced body weight gain, and an increase in glucose and insulin tolerance tests (AUCs). [18] All rats underwent plasma insulin tolerance test, conscious cystometry, leak-point pressure (LPP) assessment, and immunohistochemical studies. [19] After male C57BL/6J mice were exposed to arsenite (0 or 20 ppm) in drinking water for 12 months, intraperitoneal glucose tolerance tests (IPGTTs) and insulin tolerance tests (ITTs) revealed an arsenite-induced glucose metabolism disorder. [20] This has been demonstrated by the glucose tolerance and insulin tolerance test. [21] Our results showed that the ginsenoside Ro (90mg/kg) treatment ameliorated body weight and lipid accumulation in multiple metabolic organs of high-fat diet–induced obese (DIO) mice without affecting food intake and improved oral glucose tolerance tests, intraperitoneal insulin tolerance tests, and fasting serum glucose. [22] OBJECTIVE To determine the variations in peak growth hormone levels during insulin tolerance test (ITT) in diagnosis of growth hormone deficiency (GHD) in children presenting with short stature. [23] 30 days later, glucose tolerance test (GTT) and insulin tolerance test (ITT) were performed. [24] In previous clinical studies in induced (healthy volunteer insulin tolerance test) and intrinsic (congenital) hyperinsulinism, RZ358 showed favorable safety and PK, and glucose normalization without hyperglycemia. [25] Fasting blood glucose, fasting serum insulin, the glucose tolerance test (GTT), and the insulin tolerance test (ITT) were measured to evaluate IR of obese mice. [26] Glucose and insulin tolerance test (GTT/ITT) were performed on both chow fed or high fat diet (HFD) fed offspring to examine the glucose metabolism status. [27] Glucose homeostasis was evaluated by glucose and insulin tolerance tests. [28] Series of blood samples were collected for 6 h pulsatile GH profile, glucose tolerance test and insulin tolerance test at 5, 8, and 9 weeks of TRF, respectively. [29] Then glucose and insulin tolerance tests were conducted. [30] Before sacrifice, body weight, intraperitoneal glucose and insulin tolerance test (IP-ITT) were performed to evaluate peripheral parameters and also behavioral tests to determine cognitive decline. [31] Forskolin administration linearly decreased blood glucose levels of high-fat diet-fed mice at 90 min and total area under curve (AUC) after insulin tolerance test. [32] Insulin sensitivity was evaluated by glucose and insulin tolerance tests. [33] Aiming to study the interaction between IL-6 and counter-regulatory hormones during hypoglycemic stress we conducted an exploratory single center study involving 26 adult patients undergoing insulin tolerance test. [34] The glucose level, glucose and insulin tolerance tests showed no significant differences (Supplementary Fig. [35] Due to concerns for possible complications during an insulin tolerance test, a cosyntropin stimulation test was performed with adequate peak cortisol response at 30. [36] Afterward, blood glucose, insulin, and glycogen content were assayed, and insulin tolerance test (ITT), oral glucose tolerance test (OGTT) were performed. [37] At day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. [38] The effect of these nanoparticles on glucose and insulin response of mice was determined by glucose and insulin tolerance tests. [39] Effects of a high-fat diet were analysed by glucose tolerance and insulin tolerance tests. [40] The short synacthen test (SST) is the most commonly performed investigation to assess adrenal function1,2 as it is more practical than the ‘gold standard’ insulin tolerance test (ITT). [41] Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT) were used to assess pre-diabetic status. [42] Prolastin-treated mice fed a HFD had improved insulin sensitivity, as assessed by insulin tolerance test, and this was associated with higher insulin-dependent IRS-1 (insulin receptor substrate) and AktSer473phosphorylation, and reduced inflammation markers in WAT but not liver or muscle. [43] We observed increased insulin sensitivity in adipose tissue, corroborating the insulin tolerance test, HOMA index, and improvements in lipid profile. [44] Insulin tolerance test (ITT) measured insulin sensitivity on day 85, and mice were euthanized starting after day 100. [45] Oral glucose tolerance test (OGTT) and Insulin Tolerance Test (ITT) were performed to determine the extent of insulin resistance in HFD fed male Wistar rats. [46] Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were also performed. [47] Oral glucose tolerance test (OGTT), insulin tolerance test (ITT), fasting blood glucose (FBG), total cholesterol (TC) and triglyceride (TG) were used to assay the disorder of glycolipid metabolism. [48] CAF-TR improved the glucose and insulin tolerance tests compared with CAF-SED group (AUC = 28. [49] Glucose and insulin tolerance tests were measured at baseline and end of study. [50]혈청 생화학적 매개변수를 분석하고 복강내 포도당 및 인슐린 내성 검사를 수행했습니다. [1] 인슐린 내성 검사와 포도당 내성을 사용하여 인슐린 저항성 및 포도당 불내증으로의 진행을 결정했습니다. [2] 또한 인슐린 내성 검사, 메티라폰 자극 검사 및 부신피질 자극 호르몬 자극 검사와 같이 HPA 축의 무결성을 진단하고 평가하기 위해 잘 정립된 다양한 동적 검사가 사용되었습니다. [3] 인슐린 감수성은 포도당(GTT)과 인슐린 내성 검사(ITT)로 평가되었습니다. [4] 혈당 수치는 또한 복강 내 포도당 내성 및 인슐린 내성 테스트를 사용하여 분석되었습니다. [5] 인슐린 저항성을 평가하기 위해 포도당 내성 검사와 인슐린 내성 검사가 사용되었습니다. [6] 인슐린 내성 검사(ITT) 및 HE-클램프는 4주 및 7주 동안 식이 투여 후 수행하였다. [7] 처리 30일 후, 동물을 금식하여 경구 포도당 및 인슐린 내성 시험을 수행하여 포도당 및 인슐린 수준을 추정하였다. [8] miR-1을 처리한 마우스는 체중이 감소하지 않았지만 인슐린 내성 테스트에 의해 측정된 인슐린 감수성이 개선되었습니다. [9] nan [10] 그러나 현재 인슐린 내성 검사(ITT)에 대한 코티솔 반응을 예측하기 위한 아침 혈청 코티솔에 대한 신뢰할 수 있는 데이터는 없습니다. [11] 비히클 대조군과 비교하여, 바리시티닙 치료는 인슐린 내성 테스트에 의해 조사된 인슐린 저항성을 유의하게 개선하고 생식선 주위(pAT) 및 서혜부 AT(iAT)에서 UCP1(핵심 갈변 마커) 발현을 증가시켰지만 체중 증가 및 AT 질량에는 영향을 미치지 않았습니다. [12] SOD1G93A 마우스와 야생형 한배 새끼는 질병의 발병 및 중기 단계에서 간접 열량 측정 및 복강 내 포도당/인슐린 내성 테스트를 받았습니다. [13] 수술 전 경구 포도당 내성 검사(OGTT), 인슐린 내성 검사(ITT) 및 혼합 식사 내성 검사(MMTT)는 수술 후 지정된 시점에서 반복되었습니다. [14] 그러나 IMM 그룹의 다른 시점에서의 혈장 포도당 수준은 복강 내 포도당 내성 검사(IPGTT) 및 인슐린 내성 검사(ITT)에서 CON 그룹보다 높았습니다(p < 0. [15] GH의 장기간(11주) 소비는 포도당 및 인슐린 내성 테스트에 따르면 HFD를 섭취한 마우스의 체중과 공복 혈당 농도를 감소시키는 경향이 있었고, 포도당 불내성 및 인슐린 저항성을 개선했습니다. [16] 공복 혈당을 측정하고 85일째 인슐린 내성 검사(ITT)를 수행하여 인슐린 민감도 및 포도당 흡수를 측정했습니다. [17] 당뇨병 전증 쥐는 경미한 고혈당증, 체중 증가 감소, 포도당 및 인슐린 내성 검사(AUC) 증가를 보였습니다. [18] nan [19] nan [20] 이것은 포도당 내성 및 인슐린 내성 테스트에 의해 입증되었습니다. [21] 우리의 결과는 ginsenoside Ro(90mg/kg) 치료가 음식 섭취에 영향을 미치지 않고 고지방식이 유도 비만(DIO) 마우스의 여러 대사 기관에서 체중 및 지질 축적을 개선하고 경구 내당능 시험, 복강 내 인슐린 내성 시험을 개선하는 것으로 나타났습니다. , 및 공복 혈청 글루코스. [22] 목적 저신장 소아의 성장 호르몬 결핍증(GHD) 진단 시 인슐린 내성 검사(ITT) 중 최고 성장 호르몬 수치의 변화를 확인합니다. [23] 30일 후 포도당 내성 검사(GTT)와 인슐린 내성 검사(ITT)를 시행하였다. [24] nan [25] nan [26] nan [27] 포도당 항상성은 포도당 및 인슐린 내성 테스트로 평가되었습니다. [28] nan [29] 그런 다음 포도당 및 인슐린 내성 테스트를 수행했습니다. [30] 희생 전에 체중, 복강 내 포도당 및 인슐린 내성 테스트 (IP-ITT)를 수행하여 말초 매개 변수를 평가하고 행동 테스트를 수행하여인지 저하를 결정했습니다. [31] nan [32] 인슐린 감수성은 포도당 및 인슐린 내성 검사로 평가되었습니다. [33] nan [34] 포도당 수준, 포도당 및 인슐린 내성 테스트는 유의한 차이를 나타내지 않았습니다(보충 그림 2). [35] 인슐린 내성 검사 중 합병증 가능성이 우려되어 30에서 적절한 최대 코티솔 반응으로 코신트로핀 자극 검사를 수행했습니다. [36] nan [37] nan [38] 포도당 및 마우스의 인슐린 반응에 대한 이러한 나노입자의 효과는 포도당 및 인슐린 내성 테스트에 의해 결정되었습니다. [39] nan [40] 짧은 시낙텐 검사(SST)는 '황금 표준' 인슐린 내성 검사(ITT)보다 더 실용적이기 때문에 부신 기능1,2을 평가하기 위해 가장 일반적으로 수행되는 조사입니다. [41] nan [42] HFD를 먹인 프롤라스틴 처리 마우스는 인슐린 내성 테스트로 평가한 바와 같이 인슐린 감수성이 개선되었으며, 이는 더 높은 인슐린 의존성 IRS-1(인슐린 수용체 기질) 및 AktSer473인산화와 관련되었으며 WAT의 염증 마커 감소와 관련되었지만 간이나 근육은 그렇지 않았습니다. . [43] 우리는 지방 조직에서 증가된 인슐린 감수성을 관찰했으며, 이는 인슐린 내성 테스트, HOMA 지수 및 지질 프로필의 개선을 뒷받침합니다. [44] 인슐린 내성 테스트(ITT)는 85일째에 인슐린 감수성을 측정했으며 100일째부터 마우스를 안락사시켰습니다. [45] nan [46] nan [47] nan [48] CAF-TR은 CAF-SED 그룹에 비해 포도당 및 인슐린 내성 검사를 개선했습니다(AUC = 28. [49] 혈당 및 인슐린 내성 테스트는 기준선과 연구 종료 시점에 측정되었습니다. [50]
insulin tolerance testing 인슐린 내성 검사
Metabolic profiling included insulin tolerance testing and MR for body composition. [1] Further, these mice were unable to metabolize exogenous insulin injected during insulin tolerance testing. [2] After 12 weeks, the T2D phenotype in HFD mice was confirmed via glucose and insulin tolerance testing and echoMRI, and all mice underwent SBD surgery. [3] Body mass, plasma lipids, insulin tolerance testing, hepatic triglyceride (TG) content, gene expression, and citrate synthase (CS) activity were determined. [4] Intraperitoneal insulin tolerance testing showed that M-BC and H-BC improved insulin resistance. [5] The mice underwent insulin tolerance testing and MRI for body composition. [6] Various metabolic and physiologic assays were performed on these mice, including glomerular filtration rate (GFR) testing, glucose and insulin tolerance testing, body composition analysis, and urine & serum analysis. [7] Interestingly, despite secreting less insulin, KDM5B-KO mice were able to maintain normoglycemia following oral glucose tolerance test, likely via improved insulin sensitivity, as suggested by insulin tolerance testing and phosphorylation of proteins belonging to the insulin signaling pathway. [8]대사 프로파일링에는 인슐린 내성 테스트와 체성분에 대한 MR이 포함되었습니다. [1] 또한, 이 마우스는 외인성 대사를 할 수 없었습니다. 인슐린 내성 검사 중에 주입된 인슐린. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8]
insulin tolerance compared 인슐린 내성 비교
Mice in the STZ-15 group did not show differences in body weights, blood glucose level, insulin level, and insulin tolerance compared to wild-type and control groups whereas those in the STZ-60 group presented a typical diabetes phenotype. [1] ET-1 receptor blockade significantly improved insulin tolerance compared to insulin resistant HFD mice and lowered expression of genes in epididymal white adipose tissue (eWAT) associated with insulin resistance and inflammation. [2]STZ-15 그룹의 마우스는 야생형 및 대조군과 비교하여 체중, 혈당 수치, 인슐린 수치 및 인슐린 내성에서 차이를 보이지 않은 반면 STZ-60 그룹의 마우스는 전형적인 당뇨병 표현형을 나타냈다. [1] ET-1 수용체 차단은 인슐린 저항성 HFD 마우스와 비교하여 인슐린 내성을 유의하게 개선하고 인슐린 저항성 및 염증과 관련된 부고환 백색 지방 조직(eWAT)의 유전자 발현을 낮췄습니다. [2]