&lt;p&gt;Assessment of insulin sensitivity and secretion in patients with fibrocalculous pancreatic diabetes&lt;/p&gt;

Aiswarya, Yalamanchi; Shivaprasad, C; Kolly, Anish; Atluri, Sridevi; Anupam, Biswas; Gulati, Amit

doi:10.2147/dmso.s204254

Cited by 7 publications

(3 citation statements)

References 64 publications

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“…Traditional T2DM risk factors for insulin resistance such as family history, obesity was also important in DM development in CP patients (Bellin et al, 2017). In fibrocalcific pancreatic diabetes (FCPD), although insulin secretion defects are considered major cause, the potential involvement of insulin resistance in pathogenesis has been more oftenly recognized (Dasgupta et al, 2015;Aiswarya et al, 2019). In AP, DEP was more frequently present in patients with higher disease severity of AP (Vujasinovic et al, 2014), and insulin resistance index was higher among these patients (Wu et al, 2011).…”

Section: Insulin Resistancementioning

confidence: 99%

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What’s Known and What’s to Know

Wei

Lin

et al. 2020

Front. Physiol.

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The clinical significance of diabetes arising in the setting of pancreatic disease (also known as diabetes of the exocrine pancreas, DEP) has drawn more attention in recent years. However, significant improvements still need to be made in the recognition, diagnosis and treatment of the disorder, and in the knowledge of the pathological mechanisms. The clinical course of DEP is different from type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). DEP develops in patients with previous existing exocrine pancreatic disorders which damage both exocrine and endocrine parts of pancreas, and lead to pancreas exocrine insufficiency (PEI) and malnutrition. Therefore, damage in various exocrine and endocrine cell types participating in glucose metabolism regulation likely contribute to the development of DEP. Due to the limited amount of clinical and experimental studies, the pathological mechanism of DEP is poorly defined. In fact, it still not entirely clear whether DEP represents a distinct pathologic entity or is a form of T2DM arising when β cell failure is accelerated by pancreatic disease. In this review, we include findings from related studies in T1DM and T2DM to highlight potential pathological mechanisms involved in initiation and progression of DEP, and to provide directions for future research studies.

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Section: Insulin Resistancementioning

confidence: 99%

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What’s Known and What’s to Know

Wei

Lin

et al. 2020

Front. Physiol.

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“…4A). Third, the mean fold change of I P R between normal and T2D subjects predicted by the optimized metamodel (1.64) demonstrates an overall improved agreement with the experimental measurements (1.74) [53] compared to the non-optimized metamodel (1.24) (Fig. 6).…”

Section: Resultsmentioning

confidence: 89%

BayesianOccam’s Razorto Optimize Models for Complex Systems

Wang,

Zhao,

Zheng

et al. 2024

Preprint

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Developing and optimizing models for complex systems poses challenges due to the inherent complexity introduced by multiple types of input information and sources of uncertainty. In this study, we utilize Bayesian formalism to analytically examine the propagation of probability in the modeling process and propose quantitative assessments for it. Upon which, we develop a method for optimizing models for complex systems by (i) minimizing model uncertainty; (ii) maximizing model consistency; and (iii) minimizing model complexity, following the BayesianOccam’s razorrationale. We showcase the benefits of this method by optimizing the modeling of the dynamic system of glucose-stimulated insulin secretion in pancreaticβ-cells, leading to an optimized model that demonstrates better alignment with experimental observations compared to the non-optimized one. We anticipate that this method will facilitate the construction of accurate, precise, and sufficiently simple models for diverse complex systems. It is implemented in our open-source softwareIntegrative Modeling Platform(IMP), ensuring its broad applicability.

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“…Because of its complexity, it is rarely performed in the clinical setting, and several indexes have been described as simple alternatives to its use. In this study, to evaluate beta cell function and IR at baseline, we used the following pre-surgical indexes: Homeostatic Model Assessment of Insulin Resistance, HOMA-IR (nicely correlated with euglycemic hyperinsulinemic clamp); Homeostatic Model Assessment of b-cell function, HOMA-beta (complementary to the former index, which evaluates b-cell function); Quantitative Insulin Sensitivity Check Index, QUICKI (which, like HOMA-IR, evaluates insulin sensitivity); Matsuda and DeFronzo index (that also evaluates insulin sensitivity, highly correlated with euglycemic hyperinsulinemic clamp); and Disposition Index (which is essentially a measure of the functionality of the pancreas in the intact individual and that predicts the onset of type 2 diabetes) (23)(24)(25)(26). These are built based on the following formulas:…”

Section: Clinical and Biochemical Parameters Evaluatedmentioning

confidence: 99%

Beta Cell Function as a Baseline Predictor of Weight Loss After Bariatric Surgery

et al. 2021

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BackgroundObesity is a multifactorial disease, which is strongly associated to other metabolic disorders. Bariatric surgery is the most effective treatment of morbid obesity. The role of beta cell function in weight loss after bariatric surgery is uncertain.AimTo evaluate the association between beta cell function and percentage of total body weight loss (TBWL%) 1, 2, 3, and 4 years after bariatric surgery in patients with morbid obesity.MethodsRetrospective longitudinal study in patients with morbid obesity followed in our center between January 2010 and July 2018. Patients were excluded if they had diabetes at baseline or missing data on the needed parameters. We evaluated baseline Homeostatic Model Assessment of IR, Homeostatic Model Assessment of β-cell function (HOMA-beta), Quantitative Insulin Sensitivity Check Index, and Matsuda and DeFronzo index, and TBWL% at years 1 to 4. Linear regression models were used to evaluate the association of indexes of insulin resistance with TBWL% (unadjusted and adjusted for age, sex, BMI, and type of surgery).ResultsThere were 1,561 patients included in this analysis. HOMA-beta was negatively associated with TBWL% at second, third, and fourth years post-surgery (β = −1.04 [−1.82 to −0.26], p<0.01; β = −1.16 [−2.13 to −0.19], p=0.02; β = −1.29 [−2.64 to 0.06], p=0.061, respectively). This was not observed in the first year post-surgery nor for the other indexes. Glycemia at baseline was positively associated to EWL% at second and third years post-surgery.Conclusionβ-cell function at baseline seems to be associated to long-term weight loss, explicitly after the first year post bariatric surgery. This might be a helpful predictor of weight loss in clinical practice.

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<p>Assessment of insulin sensitivity and secretion in patients with fibrocalculous pancreatic diabetes</p>

Cited by 7 publications

References 64 publications

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What’s Known and What’s to Know

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What’s Known and What’s to Know

BayesianOccam’s Razorto Optimize Models for Complex Systems

Beta Cell Function as a Baseline Predictor of Weight Loss After Bariatric Surgery

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