Cited by 133Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismCardiovascular Disease and Adiposity

The Multifaceted Roles of Adipose Tissue—Therapeutic Targets for Diabetes and Beyond: The 2015 Banting Lecture

Open access
Scherer, Philipp E.·2016·Diabetes

Abstract

The Banting Medal for Scientific Achievement is the highest scientific award of the American Diabetes Association (ADA). Given in memory of Sir Frederick Banting, one of the key investigators in the discovery of insulin, the Banting Medal is awarded annually for scientific excellence, recognizing significant long-term contributions to the understanding, treatment, or prevention of diabetes. Philipp E. Scherer, PhD, of the Touchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, TX, received the prestigious award at the ADA's 75th Scientific Sessions, 5–9 June 2015, in Boston, MA. He presented the Banting Lecture, “The Multifaceted Roles of Adipose Tissue—Therapeutic Targets for Diabetes and Beyond,” on Sunday, 7 June 2015. A number of different cell types contribute to the cellular architecture of adipose tissue. Although the adipocyte is functionally making important contributions to systemic metabolic homeostatis, several additional cell types contribute a supportive role to bestow maximal flexibility on the tissue with respect to many biosynthetic and catabolic processes, depending on the metabolic state. These cells include vascular endothelial cells, a host of immune cells, and adipocyte precursor cells and fibroblasts. Combined, these cell types give rise to a tissue with remarkable flexibility with respect to expansion and contraction, while optimizing the ability of the tissue to act as an endocrine organ through the release of many protein factors, critically influencing systemic lipid homeostasis and biochemically contributing many metabolites. Using an example from each of these categories—adiponectin as a key adipokine, sphingolipids as critical mediators of insulin sensitivity, and uridine as an important metabolite contributed by the adipocyte to the systemic pool—I will discuss the emerging genesis of the adipocyte over the past 20 years from metabolic bystander to key driver of metabolic flexibility.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.2337/db16-0339

Cites

80 of 80 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • This remodeling is characterized by changes such as modification of adipocyte area, disturbance in fatty acid turnover, rearrangement of extracellular matrix components, inflammation, and modulation of the browning phenotype.

    “This process is characterized by a set of changes, such as: modification of the adipocyte area (hypertrophy, hyperplasia or atrophy; Arner, 2000); disturbance in fatty acid turnover (lipolysis and lipogenesis; Arner et al., 2010); rearrangement of extra-cellular matrix components (Scherer, 2016); inflammation (Batista et al., 2012); modulation of the browning phenotype related to the thermogenic”
  • Cotadutide is a synthetic human oxyntomodulin-based peptide with a palmitic acid side-chain that enables albumin binding and a longer duration of action.

    “Cotadutide (also termed MEDI0382) is a synthetic peptide based on human OMX, which employs a palmitic acid side-chain91 that enables albumin binding and thus extension of its duration of action.”

    From Transforming obesity: The advancement of multi-receptor drugs (2024) · cites this paper as [91]

    The supplied passages and additional searches of our copy discuss adiponectin, adipose-tissue metabolism, and potential adiponectin-receptor therapies. They do not address cotadutide or MEDI0382, an oxyntomodulin-based peptide, or a palmitic-acid side-chain used for albumin binding and longer action. The citation therefore cannot be verified from this source. (LLM, conf=0.76)

    Experimental — accuracy not yet measured
  • In Phase 2 trials, cotadutide produced weight loss, greater hepatic lipid lowering, appetite suppression, and reductions in blood pressure and HbA1c in people with obesity and T2D.

    “In clinical studies, cotadutide was indeed well tolerated95,96, and in Phase 2 clinical trials, the peptide displayed impressive weight loss efficacy, superior hepatic lipid-lowering capabilities and appetite suppression, along with a reduction in blood pressure and HbA1c levels in individuals with obesity and T2D91,95,97.”

    From Transforming obesity: The advancement of multi-receptor drugs (2024) · cites this paper as [91]

    The supplied passages and searches for cotadutide, Phase 2 trials, and the claimed clinical outcomes found no discussion of cotadutide in this paper. The Abstract passage on reduced hepatic lipid content concerns acid ceramidase in a mouse model, not cotadutide in people with obesity and type 2 diabetes. No passage in our copy establishes the attributed trial results. (LLM, conf=0.78)

    Experimental — accuracy not yet measured
  • The extant adipocytes' impaired insulin signalling permits lipolysis, further promoting local hyperlipidaemia.

    “Furthermore, the extant adipocytes' impaired insulin signalling permits lipolysis, further promoting local hyperlipidaemia.[ 28 ]”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Scherer, P. E.
Affiliations
The University of Texas Southwestern Medical Center (US)
Corresponding author
Scherer, Philipp E.
Venue
Diabetes
Published
2016-05-18
Volume
65
Issue
6
Pages
1452-1461
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2406023708
Cited by
133
References
80
Citations by year
2026: 7 · 2025: 9 · 2024: 10 · 2023: 12 · 2022: 12 · 2021: 18 · 2020: 11 · 2019: 14 · 2018: 18 · 2017: 17 · 2016: 5
FWCI
16.88
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (P01-DK088761, R01-DK099110, R01-DK55758)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords
adipose tissue, adipocytes, adipose tissue endocrine function, adipokines, adiponectin, sphingolipids, insulin sensitivity, uridine, adipose tissue immune cells, lipid homeostasis, metabolic flexibility
MeSH terms
Adipose Tissue, Awards and Prizes, Boston, Diabetes Mellitus, Humans, Insulin Resistance, Adipocytes

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review