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Leptin Action on GABAergic Neurons Prevents Obesity and Reduces Inhibitory Tone to POMC Neurons
TLDR
This work takes an alternative approach and tests whether first-order neurons are inhibitory (GABAergic, VGAT⁺) or excitatory (glutamatergic, VGLUT2⁺), which mediates the vast majority of leptin's antiobesity effects.
Leptin Directly Activates SF1 Neurons in the VMH, and This Action by Leptin Is Required for Normal Body-Weight Homeostasis
TLDR
It is shown that leptin depolarizes and increases the firing rate of steroidogenic factor-1 (SF1)-positive neurons in the VMH, and that leptin action at this site plays an important role in reducing body weight and, of note, in resisting diet-induced obesity.
Leptin Receptor Signaling in POMC Neurons Is Required for Normal Body Weight Homeostasis
TLDR
Leptin receptors on POMC neurons are required but not solely responsible for leptin's regulation of body weight homeostasis, as tested using the Cre/loxP system.
Metabolic Dysregulation and Adipose Tissue Fibrosis: Role of Collagen VI
TLDR
It is suggested that weakening the extracellular scaffold of adipocytes enables their stress-free expansion during states of positive energy balance, which is consequently associated with an improved inflammatory profile and implicating “adipose tissue fibrosis” as a hallmark of metabolically challenged adipocytes.
Forkhead protein FoxO1 mediates Agrp-dependent effects of leptin on food intake
TLDR
Delivery of adenovirus encoding a constitutively nuclear mutant FoxO1, a transcription factor known to control liver metabolism and pancreatic beta-cell function, to the hypothalamic arcuate nucleus of rodents results in a loss of the ability of leptin to curtail food intake and suppress expression of Agrp.
Leptin acts via leptin receptor-expressing lateral hypothalamic neurons to modulate the mesolimbic dopamine system and suppress feeding.
TLDR
It is shown that leptin directly regulates a population of leptin receptor (LepRb)-expressing inhibitory neurons in the LHA and that leptin action via these LHA LepRb neurons decreases feeding and body weight in leptin-deficient animals.
Obesity, metabolic syndrome, and prostate cancer.
TLDR
Whether obesity and metabolic syndrome modulate the risk of prostate cancer through chronic inflammation needs to be investigated further.
Phenotypes of Mouse diabetes and Rat fatty Due to Mutations in the OB (Leptin) Receptor
TLDR
The cloning of ob, and the demonstration that it encodes a secreted protein that binds specifically to a receptor (OB-R) in the brain, have validated critical aspects of this hypothesis.
Nonsense mutation in the human growth hormone-releasing hormone receptor causes growth failure analogous to the little (lit) mouse
TLDR
A nonsense mutation in the human GHRHR gene is reported that results in profound GH deficiency in at least two members of a consanguineous family and may account for other instances ofGH deficiency in which the growth hormone gene is normal.
Leptin's effect on puberty in mice is relayed by the ventral premammillary nucleus and does not require signaling in Kiss1 neurons.
TLDR
It is suggested that the PMV is a key site for leptin's permissive action at the onset of puberty and support the hypothesis that the multiple actions of leptin to control metabolism and reproduction are anatomically dissociated.
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