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JCI table of contents, October 21, 2002

Researchers uncover the role of parasympathetic innervation in fat distribution, revealing functional implications for obesity. Additionally, studies explore the molecular mechanisms behind long QT-3 syndrome, immunodeficiencies, and intestinal lymphocyte recruitment, shedding light on novel therapeutic targets.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateOct 22, 2002

Forging a link between brain and bone

A recent study published in JCI Journals reveals a significant connection between the brain and bone health, with implications for osteoporosis treatment. The findings suggest that certain neurological factors contribute to the development of bone disorders, opening up new avenues for therapy.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateMar 27, 2002

Leptin replacement therapy reduces metabolic abnormalities in patients with rare fat disorders, researchers report

Researchers report significant improvements in patients with rare fat disorders who received leptin replacement therapy, including reduced triglyceride levels and liver fat accumulation. The therapy also controlled severe insulin resistance and improved blood glucose levels in most participants.

SourceUT Southwestern Medical Center·JournalNew England Journal of Medicine·DateFeb 20, 2002

Leptin and obesity: All in the head?

Research suggests that leptin, a hormone involved in weight regulation, may be more closely tied to mental factors than previously thought. Studies have found that alterations in brain structure and function may play a key role in leptin-related obesity.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateOct 10, 2001

Converging pathways regulate energy metabolism

Researchers discovered two converging pathways regulated by leptin, which modulate energy expenditure through the TRH promoter. Thyroid hormone also suppresses TRH production, integrating various signals to control energy metabolism.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateDec 31, 2000

Chipping away at leptin's effects

Scientists have identified a number of genes specifically regulated by the hormone leptin, which is produced by fat tissue and secreted into the bloodstream. These findings offer new insights into how leptin causes fat loss and decreased appetite, and may also provide new targets for drugs designed to stimulate weight loss.

SourceHoward Hughes Medical Institute·JournalGenes & Development·DateApr 14, 2000

Regulator Of Fat Thermostat Found

Researchers found that oral administration of a steroid hormone boosts circulating leptin levels in humans, with higher levels observed in obese individuals. The study suggests that overweight people still have leptin reserves and may benefit from high-dose leptin therapy.

SourceWashington University in St. Louis·JournalThe Journal of Clinical Endocrinology & Metabolism·DateDec 22, 1997

Human Breast Milk Contains Obesity Hormone

Researchers found leptin in human breast milk, which correlates with the amount of body fat in lactating mothers. The hormone may play a role in infant development and potentially influence weight gain or obesity later in life.

SourcePurdue University·JournalBiochemical and Biophysical Research Communications·DateDec 19, 1997

Resistance To Leptin Contributes To Obesity

A study published in the Proceedings of the National Academy of Sciences found that mice with resistance to leptin are more likely to become obese. The researchers used a novel technique called ICV infusion to deliver leptin directly into the brain, which resulted in significant weight loss and fat reduction in lean mice.

SourceRockefeller University·JournalProceedings of the National Academy of Sciences·DateAug 1, 1997

Low Leptin Levels In Restrained Eaters

Research reveals low leptin levels in restrained eaters, particularly in underweight females, who have higher cognitive restraint scores. The study found a negative correlation between leptin levels and cognitive restraint scores in these individuals.

SourceMolecular Psychiatry·JournalMolecular Psychiatry·DateJun 30, 1997