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Sayeepriyadarshini Anakk - One of the best experts on this subject based on the ideXlab platform.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in male mice
    Endocrinology, 2021
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Collin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that male intestine-specific Shp knockout (IShpKO) mice exhibit higher intestinal BA but not hepatic or serum BA levels compared with the f/f Shp animals when challenged with an acute (5-day) 1% cholic acid (CA) diet. We also found that BA synthetic genes Cyp7a1 and Cyp8b1 are not repressed to the same extent in IShpKO compared with control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα messenger RNA (mRNA) but increased Asbt (BA ileal uptake transporter) and Ostα (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, apical sodium-dependent bile acid transporter (ASBT) was downregulated, while organic solute transporter-α/β (OSTα/β) expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villi length and goblet cell numbers. However, no difference in villi length, and the expression of BA regulator and transporter genes, was seen between f/f Shp and IShpKO animals after a chronic (14-day) CA diet, suggesting a potential adaptive Response. We found the upregulation of the Pparα-Ugt axis after 14 days of CA diet may reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in male mice
    Endocrinology, 2021
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Collin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that male Intestine-specific Shp Knockout (IShpKO) mice exhibit higher intestinal BA but not hepatic or serum BA levels compared to the f/f Shp animals when challenged with an acute (5-day) 1% cholic acid (CA) diet. We also find that BA synthetic genes Cyp7A1 and Cyp8b1 are not repressed to the same extent in IShpKO compared to control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα mRNA but increased Asbt (BA ileal uptake transporter) and Ostα (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, ASBT was downregulated, while OSTα/β expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villi length and goblet cell numbers. However, no difference in villi length, and the expression of BA regulator and transporter genes was seen between f/f Shp and IShpKO animals after chronic (14-day) CA diet suggesting a potential adaptive Response. We found the upregulation of the Pparα-Ugt axis after 14-days of CA diet may reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in mice
    bioRxiv, 2020
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Colin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that Intestine-specific Shp knockout (IShpKO) mice have higher intestinal and hepatic BAs, but not serum BAs when challenged with an acute (5-day) 1% cholic acid (CA) diet. Consistent with this finding, BA synthetic genes Cyp7A1 and Cyp8b1 are not repressed to the same extent in IShpKO compared to control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα mRNA but increased Asbt (BA ileal uptake transporter) and Ostβ (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, ASBT was downregulated, while OSTα/β expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villus length and goblet cell numbers. However, no difference in goblet cell number, villus morphology, crypt depth, and the expression of BA regulator and transporter genes was seen between f/f Shp and IShpKO mice after chronic (14-day) CA diet suggesting an adaptive Response. We found the upregulation of the Pparα-Ugt axis, which can reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

Olivier Sitbon - One of the best experts on this subject based on the ideXlab platform.

  • long Term Response to calcium channel blockers in non idiopathic pulmonary arterial hypertension
    European Heart Journal, 2010
    Co-Authors: David Montani, Marc Humbert, Xavier Jais, Gilles Garcia, Philippe Herve, Gerald Simonneau, Laurent Savale, Delphine Natali, Olivier Sitbon
    Abstract:

    Aims To assess the acute vasodilator Response and long-Term Response to calcium-channel blockers (CCB) in pulmonary arterial hypertension (PAH) with associated conditions. Methods and results The Response to acute vasodilator testing [>20% decrease in mean pulmonary artery pressure (mPAP) and total pulmonary resistance] was assessed in 663 consecutive PAH patients with connective tissue disease (CTD; n = 168), portal hypertension (PoPH; n = 153), anorexigen use ( n = 127), human immunodeficiency virus infection (HIV; n = 124), congenital heart disease (CHD; n = 50), and pulmonary veno-occlusive disease or capillary haemangiomatosis (PVOD/PCH; n = 41). An acute vasodilator Response was observed in 13.4% of PAH-anorexigen patients, 12.2% of PVOD/PCH, 10.1% of CTD, 1.6% of HIV, 1.3% of PoPH, and was absent in CHD. A long-Term Response to CCB (marked haemodynamic improvement at 3–4 months and New York Heart Association functional class I or II after 1 year) was reported in 9.4% of PAH-anorexigen patients but was rare in HIV, PoPH, CTD (1.6, 0.7, and 0.6%, respectively) and absent in PVOD/PCH. All patients with a long-Term CCB Response were alive after 5 years; two deaths not related to PAH occurred after this time. Recent criteria for acute Response based on the fall in mPAP to <40 mmHg are more specific to detect long-Term responders to CCB. Conclusion A long-Term CCB Response was reported in patients with PAH associated with anorexigen use, but was rare in patients with PoPH or HIV and absent in PVOD/PCH, CHD, and the vast majority of CTD. The prognosis of long-Term responders was favourable and related to the underlying cause of PAH.

  • long Term Response to calcium channel blockers in idiopathic pulmonary arterial hypertension
    Circulation, 2005
    Co-Authors: Olivier Sitbon, Marc Humbert, Xavier Jais, V Ioos, A Hamid, Steeve Provencher, Gilles Garcia, Florence Parent, Philippe Herve, Gerald Simonneau
    Abstract:

    Background— Characteristics of patients with idiopathic pulmonary arterial hypertension (IPAH) who benefit from long-Term calcium channel blockers (CCB) are unknown. Methods and Results— Acute pulmonary vasodilator testing with epoprostenol or nitric oxide was performed in 557 IPAH patients. Acute responders, defined by a fall in both mean pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) >20%, received long-Term oral CCB. Patients who benefit from long-Term CCB were defined as those being in New York Heart Association (NYHA) functional class I or II after at least 1 year on CCB monotherapy. Among the 70 patients who displayed acute pulmonary vasoreactivity (12.6%; 95% CI, 9.8% to 15.3%) and received CCB therapy, only 38 showed long-Term improvement (6.8%; 95% CI, 4.7% to 8.9%). Long-Term CCB responders had less severe disease at baseline than patients who failed. During acute vasodilator testing, long-Term CCB responders displayed a more pronounced fall in mean PAP (−39±11% versus −...

Gerald Simonneau - One of the best experts on this subject based on the ideXlab platform.

  • long Term Response to calcium channel blockers in non idiopathic pulmonary arterial hypertension
    European Heart Journal, 2010
    Co-Authors: David Montani, Marc Humbert, Xavier Jais, Gilles Garcia, Philippe Herve, Gerald Simonneau, Laurent Savale, Delphine Natali, Olivier Sitbon
    Abstract:

    Aims To assess the acute vasodilator Response and long-Term Response to calcium-channel blockers (CCB) in pulmonary arterial hypertension (PAH) with associated conditions. Methods and results The Response to acute vasodilator testing [>20% decrease in mean pulmonary artery pressure (mPAP) and total pulmonary resistance] was assessed in 663 consecutive PAH patients with connective tissue disease (CTD; n = 168), portal hypertension (PoPH; n = 153), anorexigen use ( n = 127), human immunodeficiency virus infection (HIV; n = 124), congenital heart disease (CHD; n = 50), and pulmonary veno-occlusive disease or capillary haemangiomatosis (PVOD/PCH; n = 41). An acute vasodilator Response was observed in 13.4% of PAH-anorexigen patients, 12.2% of PVOD/PCH, 10.1% of CTD, 1.6% of HIV, 1.3% of PoPH, and was absent in CHD. A long-Term Response to CCB (marked haemodynamic improvement at 3–4 months and New York Heart Association functional class I or II after 1 year) was reported in 9.4% of PAH-anorexigen patients but was rare in HIV, PoPH, CTD (1.6, 0.7, and 0.6%, respectively) and absent in PVOD/PCH. All patients with a long-Term CCB Response were alive after 5 years; two deaths not related to PAH occurred after this time. Recent criteria for acute Response based on the fall in mPAP to <40 mmHg are more specific to detect long-Term responders to CCB. Conclusion A long-Term CCB Response was reported in patients with PAH associated with anorexigen use, but was rare in patients with PoPH or HIV and absent in PVOD/PCH, CHD, and the vast majority of CTD. The prognosis of long-Term responders was favourable and related to the underlying cause of PAH.

  • long Term Response to calcium channel blockers in idiopathic pulmonary arterial hypertension
    Circulation, 2005
    Co-Authors: Olivier Sitbon, Marc Humbert, Xavier Jais, V Ioos, A Hamid, Steeve Provencher, Gilles Garcia, Florence Parent, Philippe Herve, Gerald Simonneau
    Abstract:

    Background— Characteristics of patients with idiopathic pulmonary arterial hypertension (IPAH) who benefit from long-Term calcium channel blockers (CCB) are unknown. Methods and Results— Acute pulmonary vasodilator testing with epoprostenol or nitric oxide was performed in 557 IPAH patients. Acute responders, defined by a fall in both mean pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) >20%, received long-Term oral CCB. Patients who benefit from long-Term CCB were defined as those being in New York Heart Association (NYHA) functional class I or II after at least 1 year on CCB monotherapy. Among the 70 patients who displayed acute pulmonary vasoreactivity (12.6%; 95% CI, 9.8% to 15.3%) and received CCB therapy, only 38 showed long-Term improvement (6.8%; 95% CI, 4.7% to 8.9%). Long-Term CCB responders had less severe disease at baseline than patients who failed. During acute vasodilator testing, long-Term CCB responders displayed a more pronounced fall in mean PAP (−39±11% versus −...

James T Nguyen - One of the best experts on this subject based on the ideXlab platform.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in male mice
    Endocrinology, 2021
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Collin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that male intestine-specific Shp knockout (IShpKO) mice exhibit higher intestinal BA but not hepatic or serum BA levels compared with the f/f Shp animals when challenged with an acute (5-day) 1% cholic acid (CA) diet. We also found that BA synthetic genes Cyp7a1 and Cyp8b1 are not repressed to the same extent in IShpKO compared with control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα messenger RNA (mRNA) but increased Asbt (BA ileal uptake transporter) and Ostα (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, apical sodium-dependent bile acid transporter (ASBT) was downregulated, while organic solute transporter-α/β (OSTα/β) expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villi length and goblet cell numbers. However, no difference in villi length, and the expression of BA regulator and transporter genes, was seen between f/f Shp and IShpKO animals after a chronic (14-day) CA diet, suggesting a potential adaptive Response. We found the upregulation of the Pparα-Ugt axis after 14 days of CA diet may reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in male mice
    Endocrinology, 2021
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Collin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that male Intestine-specific Shp Knockout (IShpKO) mice exhibit higher intestinal BA but not hepatic or serum BA levels compared to the f/f Shp animals when challenged with an acute (5-day) 1% cholic acid (CA) diet. We also find that BA synthetic genes Cyp7A1 and Cyp8b1 are not repressed to the same extent in IShpKO compared to control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα mRNA but increased Asbt (BA ileal uptake transporter) and Ostα (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, ASBT was downregulated, while OSTα/β expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villi length and goblet cell numbers. However, no difference in villi length, and the expression of BA regulator and transporter genes was seen between f/f Shp and IShpKO animals after chronic (14-day) CA diet suggesting a potential adaptive Response. We found the upregulation of the Pparα-Ugt axis after 14-days of CA diet may reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in mice
    bioRxiv, 2020
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Colin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that Intestine-specific Shp knockout (IShpKO) mice have higher intestinal and hepatic BAs, but not serum BAs when challenged with an acute (5-day) 1% cholic acid (CA) diet. Consistent with this finding, BA synthetic genes Cyp7A1 and Cyp8b1 are not repressed to the same extent in IShpKO compared to control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα mRNA but increased Asbt (BA ileal uptake transporter) and Ostβ (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, ASBT was downregulated, while OSTα/β expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villus length and goblet cell numbers. However, no difference in goblet cell number, villus morphology, crypt depth, and the expression of BA regulator and transporter genes was seen between f/f Shp and IShpKO mice after chronic (14-day) CA diet suggesting an adaptive Response. We found the upregulation of the Pparα-Ugt axis, which can reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

Ryan Riessen - One of the best experts on this subject based on the ideXlab platform.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in male mice
    Endocrinology, 2021
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Collin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that male intestine-specific Shp knockout (IShpKO) mice exhibit higher intestinal BA but not hepatic or serum BA levels compared with the f/f Shp animals when challenged with an acute (5-day) 1% cholic acid (CA) diet. We also found that BA synthetic genes Cyp7a1 and Cyp8b1 are not repressed to the same extent in IShpKO compared with control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα messenger RNA (mRNA) but increased Asbt (BA ileal uptake transporter) and Ostα (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, apical sodium-dependent bile acid transporter (ASBT) was downregulated, while organic solute transporter-α/β (OSTα/β) expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villi length and goblet cell numbers. However, no difference in villi length, and the expression of BA regulator and transporter genes, was seen between f/f Shp and IShpKO animals after a chronic (14-day) CA diet, suggesting a potential adaptive Response. We found the upregulation of the Pparα-Ugt axis after 14 days of CA diet may reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in male mice
    Endocrinology, 2021
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Collin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that male Intestine-specific Shp Knockout (IShpKO) mice exhibit higher intestinal BA but not hepatic or serum BA levels compared to the f/f Shp animals when challenged with an acute (5-day) 1% cholic acid (CA) diet. We also find that BA synthetic genes Cyp7A1 and Cyp8b1 are not repressed to the same extent in IShpKO compared to control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα mRNA but increased Asbt (BA ileal uptake transporter) and Ostα (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, ASBT was downregulated, while OSTα/β expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villi length and goblet cell numbers. However, no difference in villi length, and the expression of BA regulator and transporter genes was seen between f/f Shp and IShpKO animals after chronic (14-day) CA diet suggesting a potential adaptive Response. We found the upregulation of the Pparα-Ugt axis after 14-days of CA diet may reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.

  • deletion of intestinal shp impairs short Term Response to cholic acid challenge in mice
    bioRxiv, 2020
    Co-Authors: James T Nguyen, Ryan Riessen, Tongyu Zhang, Colin Kieffer, Sayeepriyadarshini Anakk
    Abstract:

    Small heterodimer partner (SHP) is a crucial regulator of bile acid (BA) transport and synthesis; however, its intestine-specific role is not fully understood. Here, we report that Intestine-specific Shp knockout (IShpKO) mice have higher intestinal and hepatic BAs, but not serum BAs when challenged with an acute (5-day) 1% cholic acid (CA) diet. Consistent with this finding, BA synthetic genes Cyp7A1 and Cyp8b1 are not repressed to the same extent in IShpKO compared to control mice post-CA challenge. Loss of intestinal SHP did not alter Fxrα mRNA but increased Asbt (BA ileal uptake transporter) and Ostβ (BA ileal efflux transporter) expression even under chow-fed conditions. Surprisingly, the acute CA diet in IShpKO did not elicit the expected induction of Fgf15 but was able to maintain the suppression of Asbt, and Ostα/β mRNA levels. At the protein level, ASBT was downregulated, while OSTα/β expression was induced and maintained regardless of diet. Examination of ileal histology in IShpKO mice challenged with acute CA diet revealed reduced villus length and goblet cell numbers. However, no difference in goblet cell number, villus morphology, crypt depth, and the expression of BA regulator and transporter genes was seen between f/f Shp and IShpKO mice after chronic (14-day) CA diet suggesting an adaptive Response. We found the upregulation of the Pparα-Ugt axis, which can reduce the BA burden and compensate for the ileal SHP function. Thus, our study reveals that ileal SHP expression contributes to both overall intestinal structure and BA homeostasis.