Sleep Loss and Circadian Misalignment - Mechanisms of Insulin Resistance

The purpose of this study is to examine the impact of timed cortisol release or differently timed cortisol rhythms on insulin resistance in both men and women undergoing sleep restriction. Chronic sleep loss is highly prevalent, affecting 1 in 3 adults in the US. Chronic sleep loss causes stress which induces insulin resistance and leads to obesity and type 2 diabetes. Many factors contribute to sleep loss including shift work, environmental disturbances, sleep/circadian disorders and comorbid medical and mental health conditions. Sleep loss increases the stress hormone cortisol in the evening and decreases daytime testosterone. Examining these hormones in a controlled laboratory environment under different sleep schedules may help researchers find solutions for adults experiencing negative health consequences related to chronic sleep loss.

Study Overview

• Status: Not yet recruiting
• Conditions: Insulin Resistance; Circadian Rhythm; Shift Work Schedule; Circadian Misalignment
• Intervention / Treatment: Drug: Dextrose; Drug: insulin; Drug: Metyrapone And Hydrocortisone

Detailed Description

Sleep loss causes stress, induces insulin resistance (IR) and leads to obesity and type 2 diabetes mellitus (T2D). Sleep loss is highly prevalent, affecting 1 in 3 adults in the USA. Many factors contribute to sleep loss including extended work hours, night shift work, environmental disturbances, sleep/circadian disorders and comorbid medical and mental health conditions. Sleep loss induces changes that typify the autonomic stress response, increases the stress hormone cortisol in the evening, and decreases daytime testosterone. The investigators discovered that preventing cortisol and testosterone from changing during sleep loss, by means of a dual-hormone clamp, stabilizes metabolism and mitigates (reduces by 50%) the induction of IR. This finding unequivocally identifies cortisol and testosterone signaling to be major pathways by which sleep loss imbalances metabolic processes and triggers IR - a critical pathogenic factor for T2D. These hormonal pathways are now prime candidates for developing mechanistically informed methods to avert IR and its devastating consequences, because no other putative pathway has been verified experimentally in humans. While groundbreaking, prior findings were only in men, and actions of cortisol and testosterone could not be separated because both were manipulated together. The next step is to characterize the distinct role of cortisol signaling and its metabolomic consequences in both sexes to unveil common and sex-dependent underlying pathways. This approach is logical because IR is induced in both sexes by increasing evening cortisol, whereas IR is induced in men by decreasing testosterone, and in women by increasing testosterone.

Night shift work misaligns the timing of behavioral rhythms with the endogenous circadian rhythm, which interferes with the homeostatic regulation of sleep and often leads to sleep loss. Circadian misalignment (CM) itself induces IR, triggers metabolic changes that are observed metabolomically, and harms health. Combining CM from simulated night shift work with experimental sleep loss induces IR to a 2-fold greater extent than sleep loss alone. These findings explain why night shift workers, which comprise 10-15% of the entire workforce, are at elevated risk for developing T2D and other metabolic disorders. Whereas IR from sleep loss relates to alterations in the shape of the cortisol rhythm (an increase in evening cortisol which flattens the diurnal cortisol slope), IR from CM in night shift workers relates to misalignment of the timing of the central cortisol rhythm to peripheral signals that follow shifted behavioral cycles. The investigators hypotheses are that (a) sleep restriction and CM induce IR through changes in the shape and timing of cortisol rhythms, respectively; and (b) downstream 24-hour metabolomic and endocrine signatures characterize the putatively sex-dependent underlying metabolic and other pathways. The investigators will examine the induction of IR and the response to normalizing the cortisol rhythm during sleep restriction alone (Aim 1), or in combination with CM (Aim 2), as well as sex differences therein (Aim 3). The investigators will conduct 2 randomized experiments in a total of 48 adults (50% women) aged 18-45 y to address these 3 aims. Studies are in-laboratory for 6 days: sleep is restricted to 4 hours/night for 2 nights followed by a 24-hour constant routine protocol without sleep.

Aim 1: Reveal disruption of the natural shape of the cortisol rhythm as a distinct mechanism by which sleep restriction induces IR. In 24 adults (12 women) undergoing sleep restriction during circadian alignment (with simulated day shift schedule), the investigators will compare IR when cortisol can change freely vs when fixed by a next-generation clamp that blocks endogenous production of cortisol and exogenously adds back cortisol to replicate mid-physiological circadian and ultradian rhythms via a portable pump. The investigators will also determine the metabolomic and endocrine signatures associated with these changes under constant routine. The investigators hypothesize that (a) IR will be largely diminished when the cortisol rhythm is clamped, demonstrating a pivotal role of the shape of the cortisol rhythm in the IR-inducing effect of sleep restriction; and (b) downstream 24-hour metabolomic and endocrine signatures will elucidate underlying mechanisms specific to sleep loss.

Aim 2: Unveil timing misalignment of the cortisol rhythm vs behavior as a separate mechanism that induces IR. In another 24 adults (12 women) undergoing sleep restriction during CM (with simulated night shift schedule), the investigators will compare IR while the fixed cortisol rhythm is either misaligned or realigned to the behavioral rhythm using the clamp as in Aim 1. The investigators hypothesize that (a) IR will be diminished when the fixed cortisol rhythm is realigned with the behavioral rhythm, showing a critical role of timing of the cortisol rhythm in the IR-inducing effect of CM; and (b) downstream 24-hour metabolomic and endocrine signatures during constant routine will elucidate underlying mechanisms due to CM distinct from those due to sleep loss in Aim 1.

Aim 3: Assess sex differences in the mechanisms underlying IR. There are sex differences in the regulation of cortisol, sleep, and other hormones. The investigators hypothesize that examining metabolomic and endocrine signatures of sleep loss during simulated day shift schedules and night shift schedules will separate underlying IR mechanisms that do or do not differ by sex. The investigators maximize power by pooling data from both shift schedules (from Aims 1 and 2) to simultaneously assess induction of IR with sleep loss alone and with CM.

The importance of IR as a pathogenic factor for T2D (a disorder that causes blindness, renal failure, heart attack, stroke, and loss of limb) mandates the proposed research. The experiments will provide essential information on prime candidate pathways underlying IR through restricted sleep and circadian misalignment in both sexes. This information will guide development of mechanistically informed solutions for the millions of men and women facing high prevalence of T2D and metabolic disorders who cannot sleep more, or at night, due to life and occupational demands. The essential first step is to delineate the processes which lead to IR.

• Study Type: Interventional
• Enrollment (Estimated): 48
• Phase: Phase 4

Contacts and Locations

• Study Contact: Name: Devon A Hansen, PhD; Phone Number: 509-358-7754; Email: devon.hansen@wsu.edu
• Study Contact Backup: Name: Olivia Brooks, MS; Phone Number: 509-358-7904; Email: olivia.brooks@wsu.edu

Study Locations

• United States
  • Washington
    • Spokane, Washington, United States, 99202
      • Sleep and Performance Research Center
      • Contact: Olivia Brooks, MS; Phone Number: 509-358-7750; Email: olivia.brooks@wsu.edu
      • Contact: Devon Hansen, PhD; Phone Number: 509-358-7754; Email: devon.hansen@wsu.edu
      • Principal Investigator: Hans Van Dongen, PhD

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: Adult
• Accepts Healthy Volunteers: Yes

Description

Inclusion Criteria:

1. Must be between 18-45 years old.
2. Has a BMI of 18-25 kg/m2 stable weight over the previous 6 weeks.

3. Is physically and psychologically healthy (incl. regular menstrual cycles in women, no clinical disorders and/or illnesses). Women will be studied during the follicular phase of their menstrual cycle.

   Menstrual cycle criteria (using PMID 10941950) 18 to 25 years - Cycle variation ≤9 days 26 to 41 years - Cycle variation ≤7 days 42 to 45 years - Cycle variation ≤9 days

4. No current medical or drug treatment (to include steroids or hormones of any type including contraceptives), as assessed by questionnaire.
5. Has a negative pregnancy test (women), no clinically significant abnormalities in blood and urine, and free of traces of drugs.
6. No history of clinically relevant psychiatric illness.
7. No previous history of drug or alcohol abuse.
8. Not a current smoker.
9. No history of brain injury or of learning disability.
10. No previous adverse reaction to sleep deprivation, jet lag, shift work or any of the drugs to be administered.
11. Not vision or hearing impairment unless corrected back to normal.
12. No endocrine disorder (no abnormal thyroid function tests; no abnormal morning blood cortisol; no primary gonadal disease as indicated by serum LH or FSH concentration > 10 or > 15 IU/L, respectively; and no hyperprolactinemia indicated by prolactin > 25 μg/L).
13. No sleep or circadian disorder.
14. Has good habitual sleep with regular bedtimes (between 6 and 10 hours in duration).
15. Not extreme morning- nor extreme evening-type using Horne-Ostberg Morningness-Eveningness criteria.
16. No travel across time zones within one month of entering the study.
17. No shift work within three months of entering the study.
18. No anemia (hematocrit <38% in men, <34% in women).
19. No blood donation within the previous 8 weeks.
20. No concurrent participation in another research study.

Study Plan

How is the study designed?

Design Details

• Primary Purpose: Diagnostic
• Allocation: Randomized
• Interventional Model: Parallel Assignment
• Masking: Double

Number of Arms

4

Arms and Interventions

Participant Group / Arm	Intervention / Treatment
Active Comparator: Misaligned cortisol rhythm-night shift condition; Cortisol will be clamped with oral administration of Metyrapone, which blocks endogenous cortisol biosynthesis. A loading dose of 3,000mg will be given at 10:00 on day 2. Every 4 hours throughout the sleep restriction and sleep deprivation phases, 500mg will be administered beginning at 14:00 on day 2 and ending with a dose at 18:00 on day 5. Using a subcutaneous pump, hydrocortisone is administered here as physiological replacement, with pulses every 3 hours beginning at 10:00 on day 2. Participants assigned to the misaligned cortisol rhythm condition will receive: lowest doses (0.5mg) at 22:00 and 01:00; moderate doses (2.3mg) at 13:00, 16:00, and 19:00; and highest doses (4.0mg) at 04:00, 07:00, and 10:00. An oral 25mg dose of hydrocortisone will be given at the end of the constant routine period to prevent any future hypocortisolemia associated with the hormone clamp.	Drug: Dextrose; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,; Drug: insulin; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,; Drug: Metyrapone And Hydrocortisone; Cortisol will be clamped with oral administration of Metyrapone, which blocks endogenous cortisol biosynthesis. A loading dose of 3,000mg will be given at 10:00 on day 2. Every 4 hours throughout the sleep restriction and sleep deprivation phases, 500mg will be administered beginning at 14:00 on day 2 and ending with a dose at 18:00 on day 5. Using a subcutaneous pump, hydrocortisone is administered here as physiological replacement, with pulses every 3 hours beginning at 10:00 on day 2. Participants will receive 3 tiers of doses: low (0.5mg), moderate (2.3mg) and high (4.0mg), the timing of which is specified by their condition assignment. For all participants, an oral 25mg dose of hydrocortisone will be given at the end of the constant routine period to prevent any future hypocortisolemia associated with the hormone clamp.
Active Comparator: Realigned cortisol rhythm-night shift condition; Cortisol will be clamped with oral administration of Metyrapone, which blocks endogenous cortisol biosynthesis. A loading dose of 3,000mg will be given at 10:00 on day 2. Every 4 hours throughout the sleep restriction and sleep deprivation phases. Participants will receive their doses at a 12-hour offset from the misaligned condition, with: lowest doses (0.5mg) at 10:00 and 13:00; moderate doses (2.3mg) at 01:00, 04:00, and 07:00; and highest doses (4.0mg) at 16:00, 19:00, and 22:00. The last subcutaneous dose will be administered at 19:00 on day 5. An oral 25mg dose of hydrocortisone will be given at the end of the constant routine period to prevent any future hypocortisolemia associated with the hormone clamp.	Drug: Dextrose; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,; Drug: insulin; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,; Drug: Metyrapone And Hydrocortisone; Cortisol will be clamped with oral administration of Metyrapone, which blocks endogenous cortisol biosynthesis. A loading dose of 3,000mg will be given at 10:00 on day 2. Every 4 hours throughout the sleep restriction and sleep deprivation phases, 500mg will be administered beginning at 14:00 on day 2 and ending with a dose at 18:00 on day 5. Using a subcutaneous pump, hydrocortisone is administered here as physiological replacement, with pulses every 3 hours beginning at 10:00 on day 2. Participants will receive 3 tiers of doses: low (0.5mg), moderate (2.3mg) and high (4.0mg), the timing of which is specified by their condition assignment. For all participants, an oral 25mg dose of hydrocortisone will be given at the end of the constant routine period to prevent any future hypocortisolemia associated with the hormone clamp.
Active Comparator: Fixed cortisol shape condition- day shift condition; Cortisol will be clamped with oral administration of Metyrapone, which blocks endogenous cortisol biosynthesis. A loading dose of 3,000mg will be given at 10:00 on day 2. Every 4 hours throughout the sleep restriction and sleep deprivation phases, 500mg will be administered beginning at 14:00 on day 2 and ending with a dose at 06:00 on day 5. Using a subcutaneous pump, hydrocortisone is administered here as physiological replacement, with pulses every 3 hours beginning at 10:00 on day 2. Participants assigned to the fixed cortisol shape condition will receive: lowest doses (0.5mg) at 22:00 and 01:00; moderate doses (2.3mg) at 13:00, 16:00, and 19:00; and highest doses (4.0mg) at 04:00, 07:00, and 10:00. The last subcutaneous dose will be administered at 07:00 on day 5. An oral 25mg dose of hydrocortisone will be given at the end of the constant routine period to prevent any future hypocortisolemia associated with the hormone clamp.	Drug: Dextrose; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,; Drug: insulin; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,; Drug: Metyrapone And Hydrocortisone; Cortisol will be clamped with oral administration of Metyrapone, which blocks endogenous cortisol biosynthesis. A loading dose of 3,000mg will be given at 10:00 on day 2. Every 4 hours throughout the sleep restriction and sleep deprivation phases, 500mg will be administered beginning at 14:00 on day 2 and ending with a dose at 18:00 on day 5. Using a subcutaneous pump, hydrocortisone is administered here as physiological replacement, with pulses every 3 hours beginning at 10:00 on day 2. Participants will receive 3 tiers of doses: low (0.5mg), moderate (2.3mg) and high (4.0mg), the timing of which is specified by their condition assignment. For all participants, an oral 25mg dose of hydrocortisone will be given at the end of the constant routine period to prevent any future hypocortisolemia associated with the hormone clamp.
Placebo Comparator: Unfixed cortisol shape condition-day shift condition; Participants will receive a metyrapone placebo at times matching the doses in Condition A (i.e., at 10:00 on day 2 and continuing every 4 hours until 06:00 on day 5). Using a subcutaneous pump, placebo hydrocortisone is administered matching the doses in Condition A (i.e., with pulses every 3 hours beginning at 10:00 on day 2 until 07:00 on day 5). A placebo matching the oral hydrocortisone will be administered at 10:00 on day 5.	Drug: Dextrose; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,; Drug: insulin; The frequently sampled intravenous glucose tolerance test is performed before and after sleep restriction, and is widely used and validated. This procedure requires intravenous administration of dextrose, 300 mg/kg as a bolus at time zero. Insulin (0.03 units/kg/min) will be slowly infused intravenously over a 5 minute period from 20 to 25 minutes. Few side effects are anticipated as both doses of glucose and insulin should result in a high, but physiological peak. Administration of insulin as 5-min infusion for clinical studies (rather than bolus) reduces the max concentrations achieved. It is not uncommon for glucose to dip below fasting glycemia at some point after the insulin administration. The concentration at the nadir depends on the subject's insulin sensitivity. Return to fasting level is a function of the waning of the insulin effect (incorporated into the minimal model) as well as counterregulation (which depends on the concentration at the nadir). This can be addressed,

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Insulin resistance-Minimal Model (Si)	Insulin resistance-minimal model (Si) will be measured from the frequently sampled intravenous glucose tolerance test (FSIVGTT) and reflects glucose disposal rate during the insulin response. it will be calculated as the change from baseline (by subtraction).	Change from baseline collection.
Insulin Resistance-Homeostatic Model Assessment of Insulin Resistance (HOMA-IR)	The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) will be measured from the frequently samples intravenous glucose tolerance test (FSIVGTT) and reflects the fasting insulin resistance. It will be calculated as the change from baseline (by subtraction).	Change from baseline collection.
Insulin Resistance-Insulin Sensitivity Index (Mi)	The Insulin Sensitivity Index (Mi) will be measured from the frequently sampled intravenous glucose tolerance test (FSIVGTT). Si is calculated using the minimal model and measures whole-body insulin sensitivity. It will be calculated as the change from baseline (by subtraction).	Change from baseline collection.

Secondary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Psychomotor Vigilance Test (PVT) Lapses	The number of lapses of attention, defined as any reaction time (RTs) >500ms will be assessed during each PVT test session. Higher RTs indicate greater impairment/lower sustained attention.	From enrollment into the lab (day 1) to the end of experimentation (day 6)
Karolinska Sleepiness Scale (KSS) Scores	Subjective ratings of sleepiness will be collected on a 9-point scale ranging from 1 (extremely wide awake) to 9 (very sleepy, fighting sleep) at regular intervals throughout laboratory experimentation to assess changes in levels of sleepiness. Higher scores indicate increased sleepiness/lowered alertness.	From enrollment into the lab (day 1) to the end of experimentation (day 6)
Metabolomics	Plasma samples will be analyzed using four complementary liquid chromatography tandem mass spectrometry (LC-MS)-based methods that couple distinct metabolite extraction and LC techniques with high resolution, accurate mass (HRAM) MS profiling to provide a hybrid analysis of hundreds of metabolites of confirmed identity and thousands of LC-MS peaks from yet to be identified compounds.	Collected every 4 hours throughout a constant routine protocol (days 4-5 of experimentation).
Delta-4 steroid hormones	Delta-4 steroid hormones will be measured by liquid chromatography tandem mass spectrometry. These steroids are extracted from blood and quantified simultaneously using spiked commercially available internal standards. The steroids measured discern steroidogenic pathways and include recognized prototypical androgen (testosterone), estrogen (estradiol), progestin (progesterone), glucocorticoid (cortisol) and mineralocorticoid (aldosterone), as well as other steroids that activate multiple steroids receptors classes.	Collected every 4 hours throughout a constant routine protocol (days 4-5 of experimentation).

Collaborators and Investigators

• Sponsor: Washington State University
• Collaborators: Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center
• Investigators: Principal Investigator: Peter Liu, MBBS, PhD, Lundquist Institute of Biomedical Innovation at Harbor-UCLA Medical Center; Principal Investigator: Hans P.A. Van Dongen, PhD, Washington State University

Study record dates

Study Major Dates

• Study Start (Estimated): July 1, 2026
• Primary Completion (Estimated): March 1, 2029
• Study Completion (Estimated): July 1, 2029

Study Registration Dates

• First Submitted: March 9, 2026
• First Submitted That Met QC Criteria: March 19, 2026
• First Posted (Actual): March 27, 2026

Study Record Updates

• Last Update Posted (Actual): May 15, 2026
• Last Update Submitted That Met QC Criteria: May 12, 2026
• Last Verified: May 1, 2026

More Information

Terms related to this study

• Keywords: sleep; type 2 diabetes; insulin resistance; circadian rhythm; Shift work
• Additional Relevant MeSH Terms: Endocrine System Diseases; Metabolic Diseases; Glucose Metabolism Disorders; Diabetes Mellitus; Hyperinsulinism; Nutritional and Metabolic Diseases; Diabetes Mellitus, Type 2; Insulin Resistance; Hormones; Hormones, Hormone Substitutes, and Hormone Antagonists; Peptide Hormones; Peptides; Amino Acids, Peptides, and Proteins; Pyridines; Heterocyclic Compounds, 1-Ring; Heterocyclic Compounds; Carbohydrates; Polycyclic Compounds; Pregnanes; Steroids; Fused-Ring Compounds; Pregnenediones; Pregnenes; Sugars; 11-Hydroxycorticosteroids; Hydroxycorticosteroids; Adrenal Cortex Hormones; 17-Hydroxycorticosteroids; Insulins; Pancreatic Hormones; Proinsulin; Hexoses; Monosaccharides; Hydrocortisone; Insulin; Metyrapone; Glucose
• Other Study ID Numbers: R01HL177106 (U.S. NIH Grant/Contract)

Plan for Individual participant data (IPD)

• Plan to Share Individual Participant Data (IPD)?: UNDECIDED
• IPD Plan Description: Study data will be released via the PIs for reasonable requests or in adherence to sponsor requirements.

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: Yes
• Studies a U.S. FDA-regulated device product: No
• product manufactured in and exported from the U.S.: No