ArticleDiabetes1997
Leptin suppression of insulin secretion by the activation of ATP-sensitive K+ channels in pancreatic beta-cells.
Article in Diabetes, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 379 citations in OpenAlex.
- Leptin: role over central nervous system in epilepsy.BMC neuroscience · 2018Pooled it
- Changes in insulin sensitivity during leptin replacement therapy in leptin-deficient patients.American journal of physiology. Endocrinology and metabolism · 2008Trial
- Impact of Body Size on Preclinical Type 1 Diabetes Development and Progression.Diabetes care · 2026Review
- Immunometabolic Dysregulation in Obesity: Integrating Macrophage Polarization, Metabolic Reprogramming, and Gut Microbiota Crosstalk.Immunity, inflammation and disease · 2026Review
- Research Progress on Leptin in Metabolic Dysfunction-associated Fatty Liver Disease.Journal of clinical and translational hepatology · 2025Review
- Metabolic Responses to High-Fat Feeding and Chronic Psychological Stress Combination.Endocrinology, diabetes & metabolism · 2024Article
- Review
- TMT-Based Proteomics Analysis Revealed the Protein Changes in Perirenal Fat from Obese Rabbits.International journal of molecular sciences · 2023Article
- The Interplay of Adipokines and Pancreatic Beta Cells in Metabolic Regulation and Diabetes.Biomedicines · 2023Review
- The leptin receptor has no role in delta-cell control of beta-cell function in the mouse.Frontiers in endocrinology · 2023Article
- β-cell dynamics in type 2 diabetes and in dietary and exercise interventions.Journal of molecular cell biology · 2022Review
- Assessment of Eating Disorders and Eating Behavior to Improve Treatment Outcomes in Women with Polycystic Ovary Syndrome.Life (Basel, Switzerland) · 2022Review
- The role of leptin and low testosterone in obesity.International journal of impotence research · 2022Review
- The Head-to-Toe Hormone: Leptin as an Extensive Modulator of Physiologic Systems.International journal of molecular sciences · 2022Review
- Phosphatidylinositol-3 kinase mediates the sweet suppressive effect of leptin in mouse taste cells.Journal of neurochemistry · 2021Article
- Association of insulin resistance and leptin receptor gene polymorphism in type 2 diabetes mellitus.Journal of the Chinese Medical Association : JCMA · 2021Article
- Redox Homeostasis in Pancreatic β-Cells: From Development to Failure.Antioxidants (Basel, Switzerland) · 2021Review
- Tissue-Specific Effects of Leptin on Glucose and Lipid Metabolism.Endocrine reviews · 2021Review
- Role of Leptin in the Digestive System.Frontiers in pharmacology · 2021Review
- Leptin modulates pancreatic β-cell membrane potential through Src kinase-mediated phosphorylation of NMDA receptors.The Journal of biological chemistry · 2020Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In the genetic mutant mouse models ob/ob or db/db, leptin deficiency or resistance, respectively, results in severe obesity and the development of a syndrome resembling NIDDM. One of the earliest manifestations in these mutant mice is hyperinsulinemia, suggesting that leptin may normally directly suppress the secretion of insulin. Here, we show that pancreatic islets express a long (signal-transducing) form of leptin-receptor mRNA and that beta-cells bind a fluorescent derivative of leptin (Cy3-leptin). The expression of leptin receptors on insulin-secreting beta-cells was also visualized utilizing antisera generated against an extracellular epitope of the receptor. A functional role for the beta-cell leptin receptor is indicated by our observation that leptin (100 ng/ml) suppressed the secretion of insulin from islets isolated from ob/ob mice. Furthermore, leptin produced a marked lowering of [Ca2+]i in ob/ob beta-cells, which was accompanied by cellular hyperpolarization and increased membrane conductance. Cell-attached patch measurements of ob/ob beta-cells demonstrated that leptin activated ATP-sensitive potassium channels (K(ATP)) by increasing the open channel probability, while exerting no effect on mean open time. These effects were reversed by the sulfonylurea tolbutamide, a specific inhibitor of K(ATP). Taken together, these observations indicate an important physiological role for leptin as an inhibitor of insulin secretion and lead us to propose that the failure of leptin to inhibit insulin secretion from the beta-cells of ob/ob and db/db mice may explain, in part, the development of hyperinsulinemia, insulin resistance, and the progression to NIDDM.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.