Trajectories of the single point insulin sensitivity estimator (SPISE) in participants who developed fatty liver (grey), fatty liver plus diabetes (black) and diabetes alone (red). Blue circles and lines indicate individuals who did not develop fatty liver or diabetes (control). Estimated marginal means and 95% confidence intervals are shown. a Entire population (n = 4,853); b participants with stringently normal ALT at baseline (n = 3580). Dx diagnosis. In both a and b, SPISE in participants who developed diabetes alone was not significantly different from that in the controls. The value in those who developed fatty liver was significantly different from that in the controls throughout the observation period (P < 0.01 for all time points). The values in those who developed fatty liver plus diabetes were significantly different from the controls at all time points in a (P < 0.05 at −5 years and <0.01 for all others) and at all but −5 years in b (P < 0.01 at −4 to 0 years)

Trajectories of the single point insulin sensitivity estimator (SPISE) in participants who developed fatty liver (grey), fatty liver plus diabetes (black) and diabetes alone (red). Blue circles and lines indicate individuals who did not develop fatty liver or diabetes (control). Estimated marginal means and 95% confidence intervals are shown. a Entire population (n = 4,853); b participants with stringently normal ALT at baseline (n = 3580). Dx diagnosis. In both a and b, SPISE in participants who developed diabetes alone was not significantly different from that in the controls. The value in those who developed fatty liver was significantly different from that in the controls throughout the observation period (P < 0.01 for all time points). The values in those who developed fatty liver plus diabetes were significantly different from the controls at all time points in a (P < 0.05 at −5 years and <0.01 for all others) and at all but −5 years in b (P < 0.01 at −4 to 0 years)

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Background/objectives: It has been unknown if attenuated insulin sensitivity (Si) in non-alcoholic fatty liver disease (NAFLD) is a cause or a result. We examined the impact of attenuated Si on NAFLD evolution. Subjects/methods: We observed 4856 NAFLD- and diabetes-free participants for a mean 2.9 years. Si was indexed by single point insulin se...

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... Among these, the SPISE was developed as an easy and affordable tool for the evaluation of whole-body insulin sensitivity, which is comparable to clamp-derived M-value in sensitivity as well as specificity (19). Several studies have evaluated the SPISE in adult as well as juvenile populations (20,(41)(42)(43)(44)(45)(46). Correa-Burrows et al. assessed SPISE for its validity in diagnosing cardiometabolic risks, namely IR and metabolic syndrome, in post-pubertal Hispanic adolescents. ...
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Background Attenuated insulin-sensitivity (IS) is a central feature of pediatric non-alcoholic fatty liver disease (NAFLD). We recently developed a new index, single point insulin sensitivity estimator (SPISE), based on triglycerides, high-density-lipoprotein and body-mass-index (BMI), and validated by euglycemic-hyperinsulinemic clamp-test (EHCT) in adolescents. This study aims to assess the performance of SPISE as an estimation of hepatic insulin (in-)sensitivity. Our results introduce SPISE as a novel and inexpensive index of hepatic insulin resistance, superior to established indices in children and adolescents with obesity. Materials and Methods Ninety-nine pubertal subjects with obesity (13.5 ± 2.0 years, 59.6% males, overall mean BMI-SDS + 2.8 ± 0.6) were stratified by MRI (magnetic resonance imaging) into a NAFLD (>5% liver-fat-content; male n=41, female n=16) and non-NAFLD (≤5%; male n=18, female n=24) group. Obesity was defined according to WHO criteria (> 2 BMI-SDS). EHCT were used to determine IS in a subgroup (n=17). Receiver-operating-characteristic (ROC)-curve was performed for diagnostic ability of SPISE, HOMA-IR (homeostatic model assessment for insulin resistance), and HIRI (hepatic insulin resistance index), assuming null hypothesis of no difference in area-under-the-curve (AUC) at 0.5. Results SPISE was lower in NAFLD (male: 4.8 ± 1.2, female: 4.5 ± 1.1) than in non-NAFLD group (male 6.0 ± 1.6, female 5.6 ± 1.5; P< 0.05 {95% confidence interval [CI]: male NAFLD 4.5, 5.2; male non-NAFLD 5.2, 6.8; female NAFLD 4.0, 5.1, female non-NAFLD 5.0, 6.2}). In males, ROC-AUC was 0.71 for SPISE (P=0.006, 95% CI: 0.54, 0.87), 0.68 for HOMA-IR (P=0.038, 95% CI: 0.48, 0.88), and 0.50 for HIRI (P=0.543, 95% CI: 0.27, 0.74). In females, ROC-AUC was 0.74 for SPISE (P=0.006), 0.59 for HOMA-IR (P=0.214), and 0.68 for HIRI (P=0.072). The optimal cutoff-level for SPISE between NAFLD and non-NAFLD patients was 5.18 overall (Youden-index: 0.35; sensitivity 0.68%, specificity 0.67%). Conclusion SPISE is significantly lower in juvenile patients with obesity-associated NAFLD. Our results suggest that SPISE indicates hepatic IR in pediatric NAFLD patients with sensitivity and specificity superior to established indices of hepatic IR.
... A number of studies previously investigated the relationship between the SPISE index and insulin-derived indicators of insulin homeostasis [23,24,[36][37][38][39]; data showed that the SPISE index was comparable to Matsuda-ISI, QUICKI and HOMA-IR when used for the identification of conditions of altered insulin sensitivity in adults [23]. Moreover, lower SPISE index significantly correlated in adults or adolescents with the presence of T2D [36], metabolic syndrome [37,39], risk of cardiovascular diseases [36], non-alcoholic fatty liver disease (NAFLD) [38], abdominal obesity, higher levels of C-reactive protein (CRP) and lower levels of adiponectin [24]. ...
... A number of studies previously investigated the relationship between the SPISE index and insulin-derived indicators of insulin homeostasis [23,24,[36][37][38][39]; data showed that the SPISE index was comparable to Matsuda-ISI, QUICKI and HOMA-IR when used for the identification of conditions of altered insulin sensitivity in adults [23]. Moreover, lower SPISE index significantly correlated in adults or adolescents with the presence of T2D [36], metabolic syndrome [37,39], risk of cardiovascular diseases [36], non-alcoholic fatty liver disease (NAFLD) [38], abdominal obesity, higher levels of C-reactive protein (CRP) and lower levels of adiponectin [24]. Finally, in line with our results obtained in youths, Sagesaka et al. demonstrated that basal SPISE index was significantly lower in adults who developed T2D 10 years later in comparison to those who did not progress to diabetes, in a longitudinal investigation on over 27,000 individuals without diabetes [40]. ...
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... Thus, this study indicates that SPISE-IR should be useful and even preferred among surrogate fasting insulin resistance indexes, with the advantage of being easily available in clinical practice, using only fasting blood lipids and BMI, and without the necessity to analyze insulin or NEFA variables. Likewise, SPISE-IR should be applicable in clinical studies on treatment of cardiovascular risk factors for risk prediction of CHD, type 2 diabetes (34), non-alcoholic fatty liver disease (42), and also possibly useful for complementary evaluation of insulin resistance in obese patients suitable for gastric bypass operations. Further clinical controlled studies should be valuable to validate the clinical utility of SPISE as a biomarker, to be used in prevention of future CHD and type 2 diabetes (34), as well as in the prevention of non-alcoholic fatty liver disease (42). ...
... Likewise, SPISE-IR should be applicable in clinical studies on treatment of cardiovascular risk factors for risk prediction of CHD, type 2 diabetes (34), non-alcoholic fatty liver disease (42), and also possibly useful for complementary evaluation of insulin resistance in obese patients suitable for gastric bypass operations. Further clinical controlled studies should be valuable to validate the clinical utility of SPISE as a biomarker, to be used in prevention of future CHD and type 2 diabetes (34), as well as in the prevention of non-alcoholic fatty liver disease (42). ...
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