Pancreatic Islets of Langerhans: Adapting Cell and Molecular Biology to Changes of Metabolism

Ornellas, Fernanda; Karise, Iara; Águila, Márcia Barbosa; Mandarim-de-Lacerda, Carlos Alberto

doi:10.1007/978-3-030-53370-0_13

Cited by 3 publications

(3 citation statements)

References 92 publications

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“…In the DIO mouse model, 11 semaglutide reduced plasma lipids, liver steatosis, inflammation, and overall glucose metabolism 12 . In addition, semaglutide favored pancreatic islet cell arrangement and enhanced beta‐cell mass in obese mice 13,14 …”

Section: Introductionmentioning

confidence: 99%

“…12 In addition, semaglutide favored pancreatic islet cell arrangement and enhanced beta-cell mass in obese mice. 13,14 Liraglutide (another GLP-1 analog) effects on mouse lipid metabolism differ from semaglutide, especially regarding plasma leptin and the magnitude of changes in other metabolic markers. 15 Altogether, the evidence indicates that the liraglutide action on adipocytes can not be directly transferred to semaglutide.…”

Section: Introductionmentioning

confidence: 99%

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Semaglutide (GLP‐1 receptor agonist) stimulates browning on subcutaneous fat adipocytes and mitigates inflammation and endoplasmic reticulum stress in visceral fat adipocytes of obese mice

Martins

Marinho

Cardoso

et al. 2022

Cell Biochemistry & Function

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Semaglutide (GLP-1 agonist) was approved for treating obesity. Although the effects on weight loss and metabolism are known, the responses of adipocytes to semaglutide are yet limited. C57BL/6 male mice (n = 20/group) were fed a control diet (C) or a high-fat (HF) diet for 16 weeks and then separated into four groups (n = 10/group) for an additional four weeks: C, C diet and semaglutide, HF, and HF diet and semaglutide. Epididymal white adipose tissue (eWAT) and subcutaneous white adipose tissue (sWAT) fat pads were studied with biochemistry, immunohistochemistry/fluorescence, stereology, and reverse transcription-quantitative polymerase chain reaction. In obese mice, semaglutide reduced the fat pad masses (eWAT, −55%; sWAT, −40%), plasmatic cytokines, and proinflammatory gene expressions: tumor necrosis factor-alpha (−60%); interleukin (IL)-6 (−55%); IL-1 beta (−40%); monocyte chemoattractant protein-1 (−90%); and leptin (−80%). Semaglutide also lessened endoplasmic reticulum (ER) stress genes of activating transcription factor-4 (−85%), CCAAT enhancer-binding protein homologous protein (−55%), and growth arrest and DNA damage-inducible gene 45 (−45%). The obese mice's adipocyte hypertrophy and macrophage infiltration were equally reduced by semaglutide. Semaglutide enhanced multiloculation and uncoupled protein 1 (UCP1) labeling in obese mice: peroxisome proliferator-activated receptor-alpha (+560%) and gamma (+150%), fibronectin type III domain-containing protein 5 (+215%), peroxisome proliferator-activated receptor-alpha coactivator (+110%), nuclear respiratory factor 1 (+260%), and mitochondrial transcription factor A (+120%). Semaglutide also increased thermogenetic gene expressions for the browning phenotype maintenance: beta-3 adrenergic receptor (+520%), PR domain containing 16 (+90%), and Ucp1 (+110%). In conclusion, semaglutide showed significant beneficial effects beyond weight loss, directly on fat pads and adipocytes

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Semaglutide (GLP‐1 receptor agonist) stimulates browning on subcutaneous fat adipocytes and mitigates inflammation and endoplasmic reticulum stress in visceral fat adipocytes of obese mice

Martins

Marinho

Cardoso

et al. 2022

Cell Biochemistry & Function

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“…It is known that obesity in the mother might implicate the offspring's adverse pancreatic islet cell remodeling and altered metabolism. [36][37][38] These alterations are associated with changes in islet pro-inflammatory regulators, oxidative stress, ER stress, and beta-cell integrity in adult offspring, consequently deteriorating insulin production and glycemic control. 39,40 However, these alterations were mitigated in the offspring when the obese mother received melatonin supplements during pregnancy and lactation, which agreed with our initial hypothesis that melatonin treatment improves insulin sensitivity and glucose tolerance in mice.…”

Section: Discussionmentioning

confidence: 99%

Obese mothers supplemented with melatonin during gestation and lactation ameliorate the male offspring’s pancreatic islet cellular composition and beta-cell function

Nagagata

Ajackson

Ornellas

et al. 2023

J Dev Orig Health Dis

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Melatonin supplementation to obese mothers during gestation and lactation might benefit the pancreatic islet cellular composition and beta-cell function in male offspring adulthood. C57BL/6 females (mothers) were assigned to two groups (n = 20/each) based on their consumption in control (C 17% kJ as fat) or high-fat diet (HF 49% kJ as fat). Mothers were supplemented with melatonin (Mel) (10 mg/kg daily) during gestation and lactation, or vehicle, forming the groups (n = 10/each): C, CMel, HF, and HFMel. The male offspring were studied, considering they only received the C diet after weaning until three months old. The HF mothers and their offspring showed higher body weight, glucose intolerance, insulin resistance, and low insulin sensitivity than the C ones. However, HFMel mothers and their offspring showed improved glucose metabolism and weight loss than the HF ones. Also, the offspring’s higher expressions of pro-inflammatory markers and endoplasmic reticulum (ER) stress were observed in HF but reduced in HFMel. Contrarily, antioxidant enzymes were less expressed in HF but improved in HFMel. In addition, HF showed increased beta-cell mass and hyperinsulinemia but diminished in HFMel. Besides, the beta-cell maturity and identity gene expressions diminished in HF but enhanced in HFMel. In conclusion, obese mothers supplemented with melatonin benefit their offspring’s islet cell remodeling and function. In addition, improving pro-inflammatory markers, oxidative stress, and ER stress resulted in better glucose and insulin levels control. Consequently, pancreatic islets and functioning beta cells were preserved in the offspring of obese mothers supplemented with melatonin.

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Unraveling the interplay: exploring signaling pathways in pancreatic cancer in the context of pancreatic embryogenesis

Swain,

Narayan,

Mishra

2024

Front. Cell Dev. Biol.

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Pancreatic cancer continues to be a deadly disease because of its delayed diagnosis and aggressive tumor biology. Oncogenes and risk factors are being reported to influence the signaling pathways involved in pancreatic embryogenesis leading to pancreatic cancer genesis. Although studies using rodent models have yielded insightful information, the scarcity of human pancreatic tissue has made it difficult to comprehend how the human pancreas develops. Transcription factors like IPF1/PDX1, HLXB9, PBX1, MEIS, Islet-1, and signaling pathways, including Hedgehog, TGF-β, and Notch, are directing pancreatic organogenesis. Any derangements in the above pathways may lead to pancreatic cancer. TP53: and CDKN2A are tumor suppressor genes, and the mutations in TP53 and somatic loss of CDKN2A are the drivers of pancreatic cancer. This review clarifies the complex signaling mechanism involved in pancreatic cancer, the same signaling pathways in pancreas development, the current therapeutic approach targeting signaling molecules, and the mechanism of action of risk factors in promoting pancreatic cancer.

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Pancreatic Islets of Langerhans: Adapting Cell and Molecular Biology to Changes of Metabolism

Cited by 3 publications

References 92 publications

Semaglutide (GLP‐1 receptor agonist) stimulates browning on subcutaneous fat adipocytes and mitigates inflammation and endoplasmic reticulum stress in visceral fat adipocytes of obese mice

Semaglutide (GLP‐1 receptor agonist) stimulates browning on subcutaneous fat adipocytes and mitigates inflammation and endoplasmic reticulum stress in visceral fat adipocytes of obese mice

Obese mothers supplemented with melatonin during gestation and lactation ameliorate the male offspring’s pancreatic islet cellular composition and beta-cell function

Unraveling the interplay: exploring signaling pathways in pancreatic cancer in the context of pancreatic embryogenesis

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