SNPMiner Trials by Shray Alag


SNPMiner Trials: Clinical Trial Report


Report for Clinical Trial NCT01503164

Developed by Shray Alag, 2019.
SNP Clinical Trial Gene

Sleep, Obesity, and Metabolism in Normal and Overweight Subjects: Effects of CPAP on Glucose Metabolism

Obstructive sleep apnea affects approximately 2-4% of middle-aged adults in the general population and is associated with several medical conditions including hypertension and coronary artery. Research over the last decade has shown that obstructive sleep apnea may also increase the propensity for insulin resistance, glucose intolerance, and type 2 diabetes mellitus. Positive airway pressure (PAP) is the first line therapy for the treatment of obstructive sleep apnea. While PAP therapy has several favorable effects such as improvements in daytime sleepiness and quality of life, it is not clear whether using PAP therapy can alter metabolic risk. The overall objective of this study is to examine whether treatment of obstructive sleep apnea with positive airway pressure therapy improves glucose tolerance and insulin sensitivity. The primary hypothesis of this study is that PAP therapy of obstructive sleep apnea will improve in insulin sensitivity and glucose metabolism.

NCT01503164 Obstructive Sleep Apnea Sleep Apnea Sleep-disordered Breathing
MeSH: Apnea Sleep Apnea Syndromes Sleep Apnea, Obstructive Respiratory Aspiration
HPO: Apnea Obstructive sleep apnea Sleep apnea

2 Interventions

Name: Positive Pressure Therapy (PAP)

Description: Positive pressure therapy is the standard of care for managing obstructive sleep apnea. It entails wearing a mask that is connected to the PAP device which deliver pressure to the upper airway during sleep.

Type: Device

Positive pressure therapy (PAP)

Name: LifeStyle Counseling

Description: Subjects randomized to the lifestyle (and nutritional) counseling arm will be given advice on a balanced dietary and exercise plan.

Type: Behavioral

Lifestyle counseling


Primary Outcomes

Description: Insulin sensitivity will be determined with the insulin-modified frequently sampled intravenous glucose tolerance test (IVGTT) before and 2-months after study intervention. This test requires administration of a weight-adjusted dose of D50W as an IV bolus at time "zero". After the glucose bolus, blood samples are drawn at the scheduled times for 3-hours. At the 20-minute mark, a weight-adjusted dose of regular insulin is administered. The resulting serum is analyzed for glucose and insulin and the "minimal model" (MINMOD) will be used to derive insulin sensitivity. A low SI signifies low insulin sensitivity and high SI represents high insulin sensitivity.

Measure: Insulin Sensitivity (SI)

Time: Baseline

Description: Insulin sensitivity will be determined with the insulin-modified frequently sampled intravenous glucose tolerance test (IVGTT) before and 2-months after study intervention. This test requires administration of a weight-adjusted dose of D50W as an IV bolus at time "zero". After the glucose bolus, blood samples are drawn at the scheduled times for 3-hours. At the 20-minute mark, a weight-adjusted dose of regular insulin is administered. The resulting serum is analyzed for glucose and insulin and the "minimal model" (MINMOD) will be used to derive insulin sensitivity. A low SI signifies low insulin sensitivity and high SI represents high insulin sensitivity.

Measure: Insulin Sensitivity (SI)

Time: 2 months after intervention

Secondary Outcomes

Description: Glucose effectiveness is the ability for glucose to move intracellularly in the absence of insulin. It is a parameter that results from the MINMOD analysis of the serum glucose and insulin levels derived from the frequently sampled intravenous glucose tolerance test. Low SG indicates a lower predisposition for glucose disposal independent of any effects of insulin.

Measure: Glucose Effectiveness (SG)

Time: Baseline

Description: Glucose effectiveness is the ability for glucose to move intracellularly in the absence of insulin. It is a parameter that results from the MINMOD analysis of the serum glucose and insulin levels derived from the frequently sampled intravenous glucose tolerance test. Low SG indicates a lower predisposition for glucose disposal independent of any effects of insulin.

Measure: Glucose Effectiveness (SG)

Time: 2 months after intervention

Description: The disposition index is the mathematical product of insulin sensitivity (SI) and acute insulin response to glucose (AIRG) both of which are derived from the MINMOD analysis of the frequently sampled intravenous glucose tolerance test data. A low DI is indicative of a higher risk of developing diabetes.

Measure: Disposition Index (DI)

Time: Baseline

Description: The disposition index is the mathematical product of insulin sensitivity (SI) and acute insulin response to glucose (AIRG) both of which are derived from the MINMOD analysis of the frequently sampled intravenous glucose tolerance test data.

Measure: Disposition Index (DI)

Time: 2 months after intervention

Description: The acute insulin response to glucose (AIRG) value is derived from the MINMOD analysis of the glucose and insulin levels obtained during the frequently sampled intravenous glucose tolerance test. A low AIRG indicates decreased ability of the pancreas to secrete insulin.

Measure: Acute Insulin Response to Glucose (AIRG)

Time: Baseline

Description: The acute insulin response to glucose (AIRG) value is derived from the MINMOD analysis of the glucose and insulin levels obtained during the frequently sampled intravenous glucose tolerance test. A low AIRG indicates decreased ability of the pancreas to secrete insulin.

Measure: Acute Insulin Response to Glucose (AIRG)

Time: 2 months after intervention

Description: Endothelial function will be assessed using peripheral arterial tonometry using the Endo-PAT device. Using the EndoPat device, the relative vasoconstriction of occluded versus non-occluded arms was derived and provided the relative hyperemic index.

Measure: Endothelial Function

Time: Baseline

Description: Endothelial function will be assessed using peripheral arterial tonometry using the Endo-PAT device. Using the EndoPat device, the relative vasoconstriction of occluded versus non-occluded arms was derived and provided the relative hyperemic index.

Measure: Endothelial Function

Time: 2 month after intervention

Description: Results of the oral glucose tolerance test will be analyzed using indices derived from the serial glucose and insulin levels over the 2 hour period. This will be the area under the glucose/ insulin curves

Measure: Area Under the Curve Assessed by Oral Glucose Tolerance Test

Time: Baseline

Description: Results of the oral glucose tolerance test will be analyzed using indices derived from the serial glucose and insulin levels over a 2 hour period 2 months post intervention. This will be the area under the glucose/ insulin curves

Measure: Area Under the Curve Assessed by Oral Glucose Tolerance Test (OGTT)

Time: 2 month after intervention

Purpose: Treatment

Allocation: Randomized

Parallel Assignment


There is one SNP

SNPs


1 D50W

This test requires administration of a weight-adjusted dose of D50W as an IV bolus at time "zero". --- D50W ---



HPO Nodes


HPO:
Apnea
Genes 227
MKRN3 CEP104 GPHN TACO1 SNORD115-1 SOX9 TMEM67 TCTN3 ABCA3 AHI1 NDUFS7 AMER1 PDE6D PSAP ACADSB TMEM237 PDHA1 MYO9A PET100 ZNF423 NADK2 RPS6KA3 KIAA0586 TMEM216 SLC5A7 GBA IPW PWRN1 TCIRG1 PEX13 CHAT HMGCL NDN NDUFA2 NDUFA4 TSPYL1 ACY1 GPR101 NEB NDUFA9 NDUFA10 ZC4H2 COQ2 COLQ TRIP13 NDUFB8 GDNF MECP2 AHDC1 NDUFS1 NDUFS2 NDUFS3 SNORD116-1 NDUFV1 NDUFS4 MKS1 NDUFS8 CHRNE NDUFV2 KIAA0753 TWIST1 SLC52A3 BMP2 NEK1 FBN1 DST FBP1 CEP120 PLAA RNF125 NDUFA12 BRAF CLCN7 TECPR2 CCDC47 BTD NFIX SURF1 GLRA1 SCN2A SCN4A BUB1 VAMP1 BUB1B ARL13B NPAP1 SNX10 GLUL HRAS PEX5 HYLS1 CC2D2A KCNQ2 SYT1 RARS2 KIAA0556 PLCB4 FGFR3 GNAI3 FGFR2 PWAR1 HERC2 SLC52A2 TMEM231 PIBF1 PHOX2B CPLANE1 DNA2 BRAT1 D2HGDH TCTN1 SDHA ALPL COL3A1 HSPD1 NPHP1 DPAGT1 COL5A1 LIAS HSPG2 SCO2 TCF4 SLC25A20 FOXRED1 MAGEL2 COL13A1 RPGRIP1L NDUFAF5 OFD1 GNE HTRA2 NDUFAF2 CISD2 SFTPB PTF1A WFS1 INPP5E SH3BP2 CEP290 NDUFAF3 SLC19A3 TMEM138 LAMB2 COX15 ARMC9 SYT2 AIP TMEM107 RET RUNX2 IDS CPT2 GABBR2 IDUA SKI ECHS1 CREBBP OPA1 SLC2A1 EDN1 TOE1 ARCN1 EDN3 NDUFA11 KIF7 MKRN3-AS1 MTFMT CRYAB NDUFA13 SLC6A9 LIFR LIPT1 ARL3 TNFSF11 ATP6 DKK1 COX1 COX2 COX3 FARS2 SLC18A3 ASCL1 SLC25A1 ND1 ND2 ND3 ND4 ND5 ND6 SLC6A5 CEP41 B9D1 FLCN PLPBP TRPV4 TRNF NDUFAF6 TRNH LTBP3 TRNK TRNL1 NGLY1 SNAP25 CTNNB1 TBR1 TRNQ TRNS1 TRNS2 BUB3 TRNV TRNW KAT6B CTSD CEP57 PCCA PCCB CSPP1 AGRN TNXB SNRPN EP300 PCK1 ATP5F1A PRNP RAI1 SOD1 TCTN2
Obstructive sleep apnea
Genes 28
HRAS SLC5A7 BMP2 TRPV4 CHAT PLCB4 FGFR3 GNAI3 SYT2 SNAP25 COL13A1 IDS IDUA SKI DNA2 MYO9A CREBBP AGRN CCDC47 SLC18A3 AHDC1 NFIX SLC25A1 EP300 EDN1 ARCN1 SH3BP2 VAMP1
Sleep apnea
Genes 70
COL3A1 MKRN3 SNORD115-1 COL5A1 BMP2 TCF4 MAGEL2 COL13A1 DKK1 BRAF GNE MYO9A CCDC47 SLC18A3 ASCL1 NFIX SLC25A1 NADK2 SH3BP2 RPS6KA3 VAMP1 NPAP1 HRAS SLC5A7 IPW PWRN1 FLCN LAMB2 SYT1 TRPV4 CHAT NDN PLCB4 FGFR3 GNAI3 LTBP3 FGFR2 SYT2 NGLY1 SNAP25 AIP PWAR1 CTNNB1 RET TSPYL1 HERC2 RUNX2 SLC52A2 GPR101 IDS PHOX2B IDUA SKI DNA2 COQ2 COLQ CEP57 CREBBP AGRN AHDC1 SNRPN EP300 EDN1 SNORD116-1 ARCN1 RAI1 SOD1 TWIST1 MKRN3-AS1 SLC52A3