ATP-Sensitive Potassium Channel-Deficient Mice Show Hyperphagia but Are Resistant to Obesity
Diabetes & Metabolism Journal
;
: 219-225, 2011.
Article
in English
| WPRIM
| ID: wpr-42487
ABSTRACT
BACKGROUND:
The hypothalamus, the center for body weight regulation, can sense changes in blood glucose level based on ATP-sensitive potassium (KATP) channels in the hypothalamic neurons. We hypothesized that a lack of glucose sensing in the hypothalamus affects the regulations of appetite and body weight.METHODS:
To evaluate this hypothesis, the responses to glucose loading and high fat feeding for eight weeks were compared in Kir6.2 knock-out (KO) mice and control C57BL/6 mice, because Kir6.2 is a key component of the KATP channel.RESULTS:
The hypothalamic neuropeptide Y (NPY) analyzed one hour after glucose injection was suppressed in C57BL/6 mice, but not in Kir6.2 KO mice, suggesting a blunted hypothalamic response to glucose in Kir6.2 KO mice. The hypothalamic NPY expression at a fed state was elevated in Kir6.2 KO mice and was accompanied with hyperphagia. However, the retroperitoneal fat mass was markedly decreased in Kir6.2 KO mice compared to that in C57BL/6 mice. Moreover, the body weight and visceral fat following eight weeks of high fat feeding in Kir6.2 KO mice were not significantly different from those in control diet-fed Kir6.2 KO mice, while body weight and visceral fat mass were elevated due to high fat feeding in C57BL/6 mice.CONCLUSION:
These results suggested that Kir6.2 KO mice showed a blunted hypothalamic response to glucose loading and elevated hypothalamic NPY expression accompanied with hyperphagia, while visceral fat mass was decreased, suggesting resistance to diet-induced obesity. Further study is needed to explain this phenomenon.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Appetite
/
Potassium
/
Social Control, Formal
/
Blood Glucose
/
Body Weight
/
Neuropeptide Y
/
Hyperphagia
/
Intra-Abdominal Fat
/
KATP Channels
/
Glucose
Type of study:
Diagnostic study
Limits:
Animals
Language:
English
Journal:
Diabetes & Metabolism Journal
Year:
2011
Type:
Article
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