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Recruiting NCT03818178

Intramyocellular Fatty Acid Trafficking in Insulin Resistance States - Effects of Intestinal Delivery of Lipids

No phase Interventional Insulin Resistance

For patients and families

In plain language

An automatic summary of structured registry data. It is an orientation aid, not a substitute for the official protocol or a physician assessment.

What is being studied
The protocol lists: Intralipid, Palm Oil Emulsion, Saline.
Who it may be relevant to
Registry conditions: Insulin Resistance. Basic parameters: 18 years — 55 years · All.
What needs checking
Age, condition and sex are only basic indicators. Prior treatment, laboratory values and other mandatory requirements appear in the eligibility criteria below.
Where it takes place
United States
Next step
Save the trial, show it to the treating physician, and confirm current recruitment with the study center. Costs, documents and travel →

Overview

Muscle insulin resistance is a hallmark of upper body obesity (UBO) and Type 2 diabetes (T2DM). It is unknown whether muscle free fatty acid (FFA) availability or intramyocellular fatty acid trafficking is responsible for muscle insulin resistance, although it has been shown that raising FFA with Intralipid can cause muscle insulin resistance within 4 hours. The investigators do not understand to what extent the incorporation of FFA into ceramides or diacylglycerols (DG) affect insulin signaling and muscle glucose uptake. The investigators propose to alter the profile and concentrations of FFA of healthy, non-obese adults using an overnight, intra-duodenal palm oil infusion vs. an overnight intra-duodenal Intralipid infusion (both compared to saline control). The investigators will compare the muscle FFA storage into intramyocellular triglyceride, intramyocellular fatty acid trafficking, activation of the insulin signaling pathway and glucose disposal rates, providing the first measure of how different FFA profiles alter muscle FFA trafficking and insulin action at the whole body and cellular/molecular levels. By identifying which steps in the insulin signaling pathway are most affected, the investigators will determine the site-specific effect of ceramides and/or DG on different degrees of insulin resistance. Hypothesis 1: Palm oil infusion will result in abnormal FFA trafficking into intra-myocellular ceramides and abnormal insulin signaling. Hypothesis 2: Intralipid infusion will result in abnormal FFA trafficking into intra-myocellular saturated DG and abnormal insulin signaling.

Interventions

  • Dietary supplement Intralipid
    Half of the participants will receive either naso-duodenal infusion of intralipid or palm oil each participant will serve as their own saline control on the second study day.
  • Dietary supplement Palm Oil Emulsion
    Half of the participants will receive either naso-duodenal infusion of intralipid or palm oil each participant will serve as their own saline control on the second study day.
  • Other Saline
    All participants will serve as their own controls with a saline infusion study day.

Primary outcome measures

  • Change in fatty acid enrichment of intramyocellular signaling molecules before and after a euglycemic, hyperinsulinemic clamp [Time frame: 18 hours]

Eligibility criteria

Inclusion criteria

  • Women and Men (Women premenopausal)
  • BMI 18-27
  • Weight stable
  • Not pregnant/nursing

Exclusion criteria

  • Ischemic heart disease
  • Atherosclerotic valvular disease
  • Smokers (> 20 cigarettes per week)
  • Bilateral oophorectomy
  • Concomitant use of medications that can alter serum lipid profile (high dose fish oil, statins, niacin, fibrates, thiazolinediones, beta-blockers, atypical antipsychotics)
  • Lidocaine allergy

Criteria are shown verbatim from the registry (in English). Final eligibility is always assessed by the study center.

Healthy volunteers: Yes

Study design

Allocation
Randomized
Model
Parallel assignment
Masking
Open label
Primary purpose
Basic science

Study locations

United States · 1 center
  • Mayo Clinic — Rochester

Identifiers

NCT: NCT03818178 · 18-002520 · 5R01DK045343-27

Primary sources (government registries)

View this study on ClinicalTrials.gov ↗