Histopathological changes in rat pancreas and skeletal muscle associated with high fat diet induced insulin resistance

GÜLEN, Meltem İÇKİN; Bağla, Aysel Güven; Yavuz, Özlem; Hişmioğulları, Adnan Adil

doi:10.3109/10520295.2015.1021380

Cited by 30 publications

(21 citation statements)

References 36 publications

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“…In the histopathological aspect of pancreatic sections, our results were similar to other reports (Gulen, Bagla, Yavuz, & Hismiogullari, 2015;Vieira et al, 2013;Yan, Li, Meng, Ren, & Kou, 2006). Several studies reported that the hypertrophy of β cell mass is necessary due to the increase in metabolic demand in IR status induced by glucolipotoxicity.…”

Section: Concerning Glucose Dysregulation Several Studies Concur Withsupporting

confidence: 91%

The nutraceutical potential ofLepidium sativum L.seed flavonoid-rich extract in managing metabolic syndrome components

et al. 2018

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The present study aimed to investigate the phytochemical and pharmacological identities of a Lepidium sativum L. (LS) flavonoid‐rich extract and its beneficial effects on metabolic, hormonal, and histological status. Chemical screening, as well as high‐performance liquid chromatography with diode‐array detection (HPLC‐DAD) identified high concentrations of the main flavonoid compounds in LS crude extract such as flavonols (quercetin, kaempferol), flavones (luteolin, apigenin), and especially flavanones (naringin, naringenin). Examinations of the biochemical and histopathological aspects showed the curative effects carried by LS flavonoid‐rich extracts on high‐fat diet‐fed Wistar rats. In this study, we propose that these molecules probably exerted the bioactivity observed in the treated group through improving insulin sensitivity, dyslipidemia, inflammation, and pancreas β cell integrity. Practical applications The LS seed is widely used in traditional medicine to treat hyperglycemia and inflammation. During the traditional mixture preparation, the thermal procedures could impair the bioactions of the most interesting group of LS phytoconstituants, flavonoids. In the present study, we propose an appropriate procedure to preserve those phytochemicals and suggest them as a substitute for the management of metabolic diseases. The dried LS extract showed an incredible set of effective flavonoids, which revealed hypoglycemic, hypolipidemic, anti‐inflammatory, cytoprotective, and antidiabetic activities. Thus, LS flavonoids constitute a remarkable product to consider in pharmaceutical industry targeting diabetes and heart diseases. Due to their enormous antioxidant potential, the LS flavonoids could be also used in food engineering and cosmetic preparations. Their practical applications is however often limited by low solubility and stability in lipophilic media. Therefore, a modification of the flavonoid structure is possibly required.

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Section: Concerning Glucose Dysregulation Several Studies Concur Withsupporting

confidence: 91%

The nutraceutical potential ofLepidium sativum L.seed flavonoid-rich extract in managing metabolic syndrome components

et al. 2018

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“…The underlying mechanisms behind the observed association in NODAP are not fully understood, but one possible mechanism is increased IPFD due to elevated triglycerides [46,47]. This is supported by an animal study suggesting that a high-fat diet induces both interlobular and intralobular fat deposition [48]. Although there is little evidence on the role of fat in insulin sensitivity in the post-pancreatitis setting, a previous study showed a strong positive association between the levels of serum triglycerides and IPFD in non-selected individuals after AP (which, in theory, might have been attributed to a high BMI) [49].…”

Section: Discussionmentioning

confidence: 78%

The Relationship between Abdominal Fat Phenotypes and Insulin Resistance in Non-Obese Individuals after Acute Pancreatitis

Skudder-Hill

Cho

et al. 2020

Nutrients

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Both type 2 prediabetes/diabetes (T2DM) and new-onset prediabetes/diabetes after acute pancreatitis (NODAP) are characterized by impaired tissue sensitivity to insulin action. Although the outcomes of NODAP and T2DM are different, it is unknown whether drivers of insulin resistance are different in the two types of diabetes. This study aimed to investigate the associations between abdominal fat phenotypes and indices of insulin sensitivity in non-obese individuals with NODAP, T2DM, and healthy controls. Indices of insulin sensitivity (homeostasis model assessment of insulin sensitivity (HOMA-IS), Raynaud index, triglyceride and glucose (TyG) index, Matsuda index) were calculated in fasting and postprandial states. Fat phenotypes (intra-pancreatic fat, intra-hepatic fat, skeletal muscle fat, visceral fat, and subcutaneous fat) were determined using magnetic resonance imaging and spectroscopy. Linear regression and relative importance analyses were conducted. Age, sex, and glycated hemoglobin A1c were adjusted for. A total of 78 non-obese individuals (26 NODAP, 20 T2DM, and 32 healthy controls) were included. Intra-pancreatic fat was significantly associated with all the indices of insulin sensitivity in the NODAP group, consistently in both the unadjusted and adjusted models. Intra-pancreatic fat was not significantly associated with any index of insulin sensitivity in the T2DM and healthy controls groups. The variance in HOMA-IS was explained the most by intra-pancreatic fat (R2 = 29%) in the NODAP group and by visceral fat (R2 = 21%) in the T2DM group. The variance in the Raynaud index was explained the most by intra-pancreatic fat (R2 = 18%) in the NODAP group and by visceral fat (R2 = 15%) in the T2DM group. The variance in the TyG index was explained the most by visceral fat in both the NODAP group (R2 = 49%) and in the T2DM group (R2 = 25%). The variance in the Matsuda index was explained the most by intra-pancreatic fat (R2 = 48%) in the NODAP group and by visceral fat (R2 = 38%) in the T2DM group. The differing association between intra-pancreatic fat and insulin resistance can be used to differentiate NODAP from T2DM. Insulin resistance in NODAP appears to be predominantly driven by increased intra-pancreatic fat deposition.

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“…The obesity epidemic has become a major global health burden due to relating comorbidities such as hyperglycemia, insulin resistance, and diabetes mellitus (type 2 diabetes [T2DM]) (Ickin Gulen et al, 2015; Wanchai et al, 2018). Several studies have so far demonstrated that long term high‐fat diet (HF) consumption induces not only obesity and insulin resistance but also histopathological alterations of the pancreas, which closely resemble early phases of T2DM (Ickin Gulen et al, 2015; Swe et al, 2019). In the initial phases of T2DM, pancreatic β‐cells adapt to the increase in insulin command by expanding β‐cell mass, leading to enlarged insulin production during obesity and insulin resistance (Bernal‐Mizrachi et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Dapagliflozin ameliorates pancreatic injury and activates kidney autophagy by modulating the AMPK/mTOR signaling pathway in obese rats

Jaikumkao

Promsan

Thongnak

et al. 2021

Journal Cellular Physiology

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Chronic consumption of a high-fat diet induces obesity and impairs the ultra-structure of organs and tissues. We examined the effect of sodium-glucose cotransporter 2 (SGLT2) inhibitor-dapagliflozin on renal and pancreatic injuries in obese condition. Rats were fed a high-fat diet for 16 weeks to induce obesity. After that, dapagliflozin or vildagliptin, 1.0 or 3.0 mg/kg/day, respectively, was administered by oral gavage for 4 weeks. The effects of dapagliflozin on insulin resistance, kidney autophagy, pancreatic oxidative stress, endoplasmic reticulum (ER) stress, inflammation, and apoptosis in high-fat diet-induced obese rats were elucidated. High-fat-diet fed rats demonstrated metabolic abnormalities including increased body weight, visceral fat weight, plasma insulin, plasma cholesterol, homeostasis model assessment (HOMA) index, and TAUCg, indicating the obese-insulin resistant and glucose intolerance conditions. Also, high-fat-diet fed rats exhibited significant pancreatic injury accompanied by decreased kidney autophagy. Dapagliflozin or vildagliptin treatment for 4 weeks ameliorated pancreatic oxidative stress, ER stress, inflammation, and apoptosis and restored kidney autophagy in obese rats. Moreover, the morphology changes of the pancreas and kidney were improved in the treated groups. Interestingly, dapagliflozin showed higher efficacy than vildagliptin in improving body weight, visceral fat weight, plasma cholesterol level, and pancreatic oxidative stress in our model. Taken together, the present study demonstrated that the therapeutic effects of dapagliflozin attenuated pancreatic injury, pancreatic oxidative stress, ER stress, inflammation, apoptosis, and exerted renoprotective effects by restoring autophagic signaling in obese rats.

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Histopathological changes in rat pancreas and skeletal muscle associated with high fat diet induced insulin resistance

Cited by 30 publications

References 36 publications

The nutraceutical potential ofLepidium sativum L.seed flavonoid-rich extract in managing metabolic syndrome components

The nutraceutical potential ofLepidium sativum L.seed flavonoid-rich extract in managing metabolic syndrome components

The Relationship between Abdominal Fat Phenotypes and Insulin Resistance in Non-Obese Individuals after Acute Pancreatitis

Dapagliflozin ameliorates pancreatic injury and activates kidney autophagy by modulating the AMPK/mTOR signaling pathway in obese rats

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