Abstract:Background and Aims:Ingestion of food stimulates the secretion of incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 to ensure the proper absorption and storage of nutrients. Menin is the 67 kDa protein product of the MEN1 gene recently reported to have a role in metabolism. In this study, we will determine the regulation of menin in the proximal duodenum by food intake and diet in correlation with GIP levels in the proximal duodenum of mice after an 18 h fast foll… Show more
“…6). Interestingly, Menin was found to respond to feeding and diet in the proximal duodenum, and it plays a negatively regulatory role on the glucose-dependent insulinotropic polypeptide (GIP) by inhibiting of the PI3K/Akt signaling pathway 19 .Figure 6Mediation by Menin of milk protein synthesis through the PI3K/Akt/mTOR signaling pathway in mammary epithelial cells. Hormones such as insulin and prolactin that acts on epithelial cells modulate the MEN1 /Menin expression level in cells, which further affects the abundance of the factors involved in mTOR signaling and eventually the synthesis of milk protein.…”
Section: Discussionmentioning
confidence: 99%
“…Recent studies have suggested a possible regulatory role for MEN1 /Menin in different tissues through the PI3K/Akt/mTOR signaling pathway 17 – 19 . Menin was found to directly interact with Akt1 and suppresses its kinase activity by regulating its translocation in the cytoplasm and/or plasma membrane 20 , 21 .…”
Section: Discussionmentioning
confidence: 99%
“…6 ). Interestingly, Menin was found to respond to feeding and diet in the proximal duodenum, and it plays a negatively regulatory role on the glucose-dependent insulinotropic polypeptide (GIP) by inhibiting of the PI3K/Akt signaling pathway 19 . Figure 6 Mediation by Menin of milk protein synthesis through the PI3K/Akt/mTOR signaling pathway in mammary epithelial cells.…”
The MEN1 gene, which encodes the protein Menin, was investigated for its regulatory role in milk protein synthesis in mammary glands. Menin responds to nutrient and hormone levels via the PI3K/Akt/mTOR pathway. Bovine mammary epithelial cells and tissues were used as experimental models in this study. The results revealed that the milk protein synthesis capacity of mammary epithelial cells could be regulated by MEN1/Menin. The overexpression of Menin caused significant suppression of factors involved in the mTOR pathway, as well as milk protein κ-casein (CSNK). In contrast, a significant increase in these factors and CSNK was observed upon MEN1/Menin knockdown. The repression of MEN1/Menin on the mTOR pathway was also observed in mammary gland tissues. Additionally, MEN1/Menin was found to elicit a negative response on prolactin (PRL) and/or insulin (INS), which caused a similar downstream impact on mTOR pathway factors and milk proteins. Collectively, our data indicate that MEN1/Menin could play a regulatory role in milk protein synthesis through mTOR signaling in the mammary gland by mediating the effects of hormones and nutrient status. The discovery of Menin’s role in mammary glands suggests Menin could be potential new target for the improvement of milk performance and adjustment of lactation period of dairy cows.
“…6). Interestingly, Menin was found to respond to feeding and diet in the proximal duodenum, and it plays a negatively regulatory role on the glucose-dependent insulinotropic polypeptide (GIP) by inhibiting of the PI3K/Akt signaling pathway 19 .Figure 6Mediation by Menin of milk protein synthesis through the PI3K/Akt/mTOR signaling pathway in mammary epithelial cells. Hormones such as insulin and prolactin that acts on epithelial cells modulate the MEN1 /Menin expression level in cells, which further affects the abundance of the factors involved in mTOR signaling and eventually the synthesis of milk protein.…”
Section: Discussionmentioning
confidence: 99%
“…Recent studies have suggested a possible regulatory role for MEN1 /Menin in different tissues through the PI3K/Akt/mTOR signaling pathway 17 – 19 . Menin was found to directly interact with Akt1 and suppresses its kinase activity by regulating its translocation in the cytoplasm and/or plasma membrane 20 , 21 .…”
Section: Discussionmentioning
confidence: 99%
“…6 ). Interestingly, Menin was found to respond to feeding and diet in the proximal duodenum, and it plays a negatively regulatory role on the glucose-dependent insulinotropic polypeptide (GIP) by inhibiting of the PI3K/Akt signaling pathway 19 . Figure 6 Mediation by Menin of milk protein synthesis through the PI3K/Akt/mTOR signaling pathway in mammary epithelial cells.…”
The MEN1 gene, which encodes the protein Menin, was investigated for its regulatory role in milk protein synthesis in mammary glands. Menin responds to nutrient and hormone levels via the PI3K/Akt/mTOR pathway. Bovine mammary epithelial cells and tissues were used as experimental models in this study. The results revealed that the milk protein synthesis capacity of mammary epithelial cells could be regulated by MEN1/Menin. The overexpression of Menin caused significant suppression of factors involved in the mTOR pathway, as well as milk protein κ-casein (CSNK). In contrast, a significant increase in these factors and CSNK was observed upon MEN1/Menin knockdown. The repression of MEN1/Menin on the mTOR pathway was also observed in mammary gland tissues. Additionally, MEN1/Menin was found to elicit a negative response on prolactin (PRL) and/or insulin (INS), which caused a similar downstream impact on mTOR pathway factors and milk proteins. Collectively, our data indicate that MEN1/Menin could play a regulatory role in milk protein synthesis through mTOR signaling in the mammary gland by mediating the effects of hormones and nutrient status. The discovery of Menin’s role in mammary glands suggests Menin could be potential new target for the improvement of milk performance and adjustment of lactation period of dairy cows.
“…In the developing stomach, fasting stimulates cell proliferation [138,139] and though corticosterone has been described as part of such effect [140], MAPK action has not been identified yet. In the proximal duodenum, feeding regulates the expression of menin (a 67 kDa protein involved in metabolic control and tumor progression), that in turn inhibits PI3K-Akt signaling, resulting in decreased glucagon-like peptide 1 (GLP-1) secretion and reduced glucose-stimulated insulin release [141]. MAPKs are combined to these pathways in the control of glucose levels, especially through JNK that is extremely decreased or even lost in insulin-resistance [142,143].…”
Section: Nutritional Influence On Cell Signalingmentioning
Mitogen-activated protein kinase (MAPK) pathways are activated by several stimuli and transduce the signal inside cells, generating diverse responses including cell proliferation, differentiation, migration and apoptosis. Each MAPK cascade comprises a series of molecules, and regulation takes place at different levels. They communicate with each other and with additional pathways, creating a signaling network that is important for cell fate determination. In this review, we focus on ERK, JNK, p38 and ERK5, the major MAPKs, and their interactions with PI3K-Akt, TGFβ/Smad and Wnt/β-catenin pathways. More importantly, we describe how MAPKs regulate cell proliferation and differentiation in the rapidly renewing epithelia that lines the gastrointestinal tract and, finally, we highlight the recent findings on nutritional aspects that affect MAPK transduction cascades.
“…The SG þ TB is similar to the duodenal switch (DS) but does not completely exclude the duodenum in order to minimize nutritional complications. The SG þ TB amplifies the nutritive stimulation of the distal gut while diminishing the exposure of the proximal bowel to nutrients without excluding the duodenum and jejunum as has been reported in the literature [5][6][7][8][9][10].…”
Background Single anastomosis sleeve ileal (SASI) bypass is a newly introduced bariatric and metabolic procedure. The present multicenter study aimed to evaluate the efficacy of the SASI bypass in the treatment of patients with morbid obesity and the metabolic syndrome. Methods This is a retrospective, seven-country, multicenter study on patients with morbid obesity who underwent the SASI bypass. Data regarding patients' demographics, body mass index (BMI), percentage of total weight loss (%TWL), percentage of excess weight loss (%EWL), and improvement in comorbidities at 12 months postoperatively and postoperative complications were collected. Results Among 605 patients who underwent the SASI, 54 were excluded and 551 (390; 70.8% female) were included. At 12 months after the SASI, a significant decrease in the BMI was observed (43.2 ± 12.5 to 31.2 ± 9.7 kg/m 2 ; p < 0.0001). The %TWL was 27.4 ± 13.4 and the %EWL was 63.9 ± 29.5. Among the 279 patients with type 2 diabetes mellitus (T2DM), complete remission was recorded in 234 (83.9%) patients and partial improvement in 43 (15.4%) patients. Eighty-six (36.1%) patients with hypertension, 104 (65%) patients with hyperlipidemia, 37 (57.8%) patients with sleep apnea, and 70 (92.1%) patients with GERD achieved remission. Fifty-six (10.1%) complications and 2 (0.3%) mortalities were recorded. Most complications were minor. All patients had 12 months follow-up. Conclusions The SASI bypass is an effective bariatric and metabolic surgery that achieved satisfactory weight loss and improvement in medical comorbidities, including T2DM, hypertension, sleep apnea, and GERD, with a low complication rate.
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