Liraglutide alters DPP4 in the circumvallate papillae of type 2 diabetic rats

Cao, Xun; Zhou, Xiao; Liu, Xiaomin; Zhou, Lihong

doi:10.1530/jme-16-0001

Cited by 5 publications

(4 citation statements)

References 32 publications

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“…Liraglutide upregulated the expressions of DPP-IV in taste buds and downregulated the same in the hypothalamus of T2DM rats. 8 Our study has also shown the effect of Liraglutide on DPP-IV activity. It significantly reduces the activity of DPP-IV in plasma of day 1 and day 21 group.…”

Section: Resultssupporting

confidence: 52%

GLP 1 Regulated Intestinal Cell’s Insulin Expression and Selfadaptation before the Onset of Type 2 Diabetes

et al. 2019

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Purpose: Basically insulin is known to be secreted by β cells of the pancreas. Recently, it has also been found to be produced and expressed by intestinal epithelial cells with the help of L cells secreting glucagon like peptide 1 (GLP 1). Here, we have studied the same intestinal insulin expression property in T2D rats. Methods: Following 2 weeks of high fat diet (HFD) consumption, we have been given a single dose of streptozotocin (STZ) (35 mg/kg bw). Rats were then sacrificed after 1, 7 and 21 days. The GLP 1 analogue, liraglutide was also given to one group of diabetic rats, upto their respective durations. Intestinal cells apoptosis were checked by tunnel assay, Incretin hormones secretion and dipeptidyl peptidase 4 (DPP-IV) activity were analyzed through ELISA and immunohistochemistry was used to determine the insulin expression of intestine at different time interval during diabetes progression. Results: As compared to 1 and 21 days, we have found minor cells apoptosis in 7 days group along with high level of GLP 1 in diabetic model. Further, these effects were enhanced by liraglutide. In response to these we have found, decreased insulin expression after 21 days and with no significant effect upto 7 days in diabetic control groups. In contrast to this, GLP-1 level and insulin expression enhances prominently after 7 days of liraglutide treatment. Conclusion: These results explain the self-adapting approach of intestinal cells against diabetes onset and insulin expression enhancing property of liraglutide under stressful conditions. This study should be continued in future for the development of intestinal insulin producing drugs, to control diabetes under irreversible β cells damage.

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Section: Resultssupporting

confidence: 52%

GLP 1 Regulated Intestinal Cell’s Insulin Expression and Selfadaptation before the Onset of Type 2 Diabetes

et al. 2019

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“…This study exhibited the liraglutide administration in the constructed IR animal and cell models, and confirm that liraglutide had a good therapeutic effect in obesity-associated IR. Previous studies have reported the regulatory effect of liraglutide on the expression of DPP4 in T2DM 28. In the current study, we observed that the increased DPP4 in the adipose tissues and adipocytes under IR status was significantly reduced by the treatment of liraglutide, which is consistent with the previous study.…”

Section: Discussionsupporting

confidence: 92%

“…Liraglutide is a kind of incretin-based drug, which has been widely used in the treatment of T2DM with obesity 27. Cao et al indicated that liraglutide administration in T2DM resulted in abnormal DPP4 expression 28. Our previous studies have reported that AMPK was up-regulated in adipocyte with liraglutide in db/db mice 29.…”

Section: Introductionmentioning

confidence: 99%

<p>Dysregulation of DPP4 Is Associated with the AMPK/JAK2/STAT3 Pathway in Adipocytes Under Insulin Resistance Status and Liraglutide Intervention</p>

Cheng

Yuan

et al. 2019

DMSO

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PurposeDipeptidyl peptidase 4 (DPP4) is one of the newly identified adipokines, which acts as paracrine in adipose tissue and as endocrine hormones in the liver, muscles and central nervous system. Expression of DPP4 was significantly upregulated in obese patients upon insulin resistance (IR) conditions, but the mechanism underlying the dysregulation of DPP4 remains unclear. This study aimed to investigate the DPP4 expression in adipose tissue and adipocytes under IR conditions or with liraglutide intervention, and explore the potential molecular mechanisms.MethodsObesity-associated IR animal and cell models were, respectively, constructed by using high-fat diet and palmitic acid (PA) stimulation. Expression of DPP4 in adipose tissues and adipocytes was estimated by quantitative real-time RT-PCR and Western-blot. Effects of the AMPK/JAK2/STAT3 pathway on DPP4 were examined by regulating the activity of AMPK and the JAK2/STAT signaling. The therapeutic efficacy of liraglutide in the IR models was evaluated, and its regulatory effects on DPP4 expression and the underlying molecular mechanisms were explored.ResultsThe expression of DPP4 was markedly upregulated in both the animal and cell IR models. In the adipocyte, DPP4 expression was found to be suppressed by the activation of AMPK, and this inhibition effect was mediated by the JAK2/STAT3 signaling. Moreover, liraglutide could alleviate the obesity-induced IR, and led to the downregulation of DPP4 in IR animal and cell models. Liraglutide intervention resulted in the activation of AMPK and deactivation of the JAK2/STAT3 signaling in the adipocytes.ConclusionTaken together, the expression of DPP4 is upregulated in adipose tissues and adipocytes upon IR conditions, but is reduced after liraglutide intervention. The dysregulation of DPP4 in the adipocytes may be performed by the AMPK/JAK2/STAT3 pathway.

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“…Initially, it was believed that TBs do not express an enzyme DPP4 that rapidly catabolizes active GLP-1 [24]. Later, DPP-4 immunoreactive cells localized in the rat taste buds with significantly higher expression of DPP-4 mRNA in the rats with diabetes [74].…”

Section: Glp-1 In the Taste Budsmentioning

confidence: 99%

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

Jensterle

Rizzo

2021

IJMS

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Preclinical studies provided some important insights into the action of glucagon-like peptide 1 (GLP-1) in taste perception. This review examines the literature to uncover some molecular mechanisms and connections between GLP-1 and the gustatory coding. Local GLP-1 production in the taste bud cells, the expression of GLP-1 receptor on the adjacent nerves, a functional continuum in the perception of sweet chemicals from the gut to the tongue and an identification of GLP-1 induced signaling pathways in peripheral and central gustatory coding all strongly suggest that GLP-1 is involved in the taste perception, especially sweet. However, the impact of GLP-1 based therapies on gustatory coding in humans remains largely unaddressed. Based on the molecular background we encourage further exploration of the tongue as a new treatment target for GLP-1 receptor agonists in clinical studies. Given that pharmacological manipulation of gustatory coding may represent a new potential strategy against obesity and diabetes, the topic is of utmost clinical relevance.

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Liraglutide alters DPP4 in the circumvallate papillae of type 2 diabetic rats

Cited by 5 publications

References 32 publications

GLP 1 Regulated Intestinal Cell’s Insulin Expression and Selfadaptation before the Onset of Type 2 Diabetes

GLP 1 Regulated Intestinal Cell’s Insulin Expression and Selfadaptation before the Onset of Type 2 Diabetes

<p>Dysregulation of DPP4 Is Associated with the AMPK/JAK2/STAT3 Pathway in Adipocytes Under Insulin Resistance Status and Liraglutide Intervention</p>

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

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