Lipid-induced Insulin Resistance: Molecular Mechanisms and Clinical Implications
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Expires on Dec 31, 2024
Credit Offered
1 AMA PRA Category 1 Credit
1 ABIM-MOC Point
1 Participation Credit
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This webinar is a live recording of the presentation. Questions about the talk and additional discussion are welcome. Please utilize the discussion forum to contact the speaker.

Metabolically unhealthy white adipose tissue (WAT) talks to the other insulin target tissues. Storage of excessive nutrients in the adipose tissue leads to inflammatory response and insulin resistance. Intracellular lipid accumulation in adipocytes causes a pro-inflammatory response through hypoxia and endoplasmic reticulum (ER) stress, eventually resulting in apoptosis. In addition, endotoxins and free fatty acids (FFAs), in association with Fetuin-A, a hepatokine, activate Toll-like receptor 4 (TLR4) in tha adipocytes and immune cells, which in turn produce a broad range of proinflammatory cytokines and chemokines — i.e.,  TNF-a, IL‑1β, IL‑8 and MCP1 — that, in turn, promote macrophage and T cell accumulation in adipose tissues. In macrophages, hyperglycaemia, lipids and endotoxins promote the formation of inflammasomes that activate IL‑1β. Adipose recruitment and activation of Plasmacytoid Dendritic Cells Fuel metaflammation. Amrit Raj Ghosh [Diabetes 2016]. Extracelllular DNA from damaged adipose tissue activates receptor for AGE (RAGE) on the plasma membrane of the plasmacytoid dendritic cells. This AGE- RAGE interaction then activates toll-like receptor 9 (TLR9) on the pDCs, leading to the production of type I interferons, that in turn induce proinflammatory polarization of resident macrophages in the adipose tissue.

Adipose tissue is a potential target in the treatment of diabesity. Cross talk between inflammed adipocytes and macrophages. Islet cells and macrophages cross talk in type 2 diabetes. Fetuin-A promotes adipose tissue inflammation. The battle against diabesity continues. There is an unmet need to address adipose tissue inflammation and insulin resistance. Lipid induced insulin resistance results in a proinflammatory state. Fetuin-A acts as an adaptor protein between FFA and TLR-4 on the surface of adipocytes and immune cells to enhance the production of proinflammatory cytokines that lead to insulin resistance in the target tissues. [Mukhopadhyay Satinath, Diabetologia, 2014]. Targeting the FFA- FetA- TLR4 pathway and adipose tissue macrophage polarization may offer novel approaches to treat lipid induced insulin resistance and T2DM. Pal D, Nature Medicine, 2012].

This presentation is intended for Fellows, Residents, Clinical and Scientific Researchers. 
  • Dietary lipids activate the TLR4–NFκB pathway in adipocytes and immune cells to produce proinflammatory cytokines that cause insulin resistance (IR).
  • Fet A acts as an adaptor protein between FFA & TLR4
  • FetA & Chemerin represent potentially new targets in the treatment of lipid-induced insulin resistance and T2DM
  • Anti-inflammatory approaches to prevent IR are attractive but may lead to unwanted inhibition of immune functions.
  • More specific treatment approaches are therefore of great interest.

The Endocrine Society is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Endocrine Society has achieved Accreditation with Commendation.

AMA PRA Category 1 Credit
The Endocrine Society designates each activity in this course for a maximum of 1.00 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. While offering CME credits noted above, this program is not intended to provide extensive training or certification in the field.

Please note that while other accrediting bodies accept AMA PRA Category 1 credit, we can only award and report this credit for MDs/DOs. For those outside of this accreditation, please complete the participation evaluation and use that certificate as proof of attendance to submit to your accrediting body.

Maintenance of Certification (MOC) - if eligible
Successful completion of each CME activity in this course, which includes participation in the evaluation component, enables the participant to earn up to 1.00 points in the American Board of Internal Medicine (ABIM) Maintenance of Certification (MOC) program. Participants will earn MOC points equivalent to the amount of CME credits claimed for the activity. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting ABIM MOC credit.

For questions about content or obtaining CME credit, please contact the Endocrine Society at

Satinath Mukhopadhyay, MD DM, FRCP (London), FAMS (India)
Professor, Department of Endocrinology & Metabolism, 
Institute of Postgraduate Medical Education & Research, Kolkata, India

As a provider of CME accredited by the Accreditation Council for Continuing Medical Education, the Endocrine Society has a policy of ensuring that the content and quality of this educational activity are balanced, independent, objective, and scientifically rigorous. The scientific content of this activity was developed under the supervision of the Endocrine Society’s peer reviewers.

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The Endocrine Society has reviewed these relationships to determine which are relevant to the content of this activity and resolved any identified conflicts of interest for these individuals.

The faculty reported no relevant financial relationships.

The Endocrine Society staff report no relevant financial relationships.

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