Differential effects of leptin on adiponectin expression with weight gain versus obesity
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00068472" target="_blank" >RIV/00159816:_____/16:00068472 - isvavai.cz</a>
Result on the web
<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747836/pdf/nihms718023.pdf" target="_blank" >https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747836/pdf/nihms718023.pdf</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/ijo.2015.181" target="_blank" >10.1038/ijo.2015.181</a>
Alternative languages
Result language
angličtina
Original language name
Differential effects of leptin on adiponectin expression with weight gain versus obesity
Original language description
BACKGROUND/OBJECTIVE: Adiponectin exerts beneficial effects by reducing inflammation and improving lipid metabolism and insulin sensitivity. Although the adiponectin level is lower in obese individuals, whether weight gain reduces adiponectin expression in humans is controversial. We sought to investigate the role of weight gain, and consequent changes in leptin, on altering adiponectin expression in humans. METHODS/RESULTS: Forty-four normal-weight healthy subjects were recruited (mean age 29 years; 14 women) and randomized to either gain 5% of body weight by 8 weeks of overfeeding (n = 34) or maintain weight (n = 10). Modest weight gain of 3.8 +/- 1.2 kg resulted in increased adiponectin level (P = 0.03), whereas weight maintenance resulted in no changes in adiponectin. Further, changes in adiponectin correlated positively with changes in leptin (P = 0.0085). In-vitro experiments using differentiated human white preadipocytes showed that leptin increased adiponectin mRNA and protein expression, whereas a leptin antagonist had opposite effects. To understand the role of leptin in established obesity, we compared adipose tissue samples obtained from normal-weight versus obese subjects. We noted, first, that leptin activated cellular signaling pathways and increased adiponectin mRNA in the adipose tissue from normal-weight participants, but did not do so in the adipose tissue from obese participants. Second, we noted that obese subjects had increased caveolin-1 expression, which attenuates leptin-dependent increases in adiponectin. CONCLUSIONS: Modest weight gain in healthy individuals is associated with increases in adiponectin levels, which correlate positively with changes in leptin. In vitro, leptin induces adiponectin expression, which is attenuated by increased caveolin-1 expression. In addition, the adipose tissue from obese subjects shows increased caveolin-1 expression and impaired leptin signaling. This leptin signal impairment may prevent concordant increases in adiponectin levels in obese subjects despite their high levels of leptin. Therefore, impaired leptin signaling may contribute to low adiponectin expression in obesity and may provide a target for increasing adiponectin expression, hence improving insulin sensitivity and cardio-metabolic profile in obesity.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30202 - Endocrinology and metabolism (including diabetes, hormones)
Result continuities
Project
<a href="/en/project/ED1.100%2F02%2F0123" target="_blank" >ED1.100/02/0123: St. Anne´s University Hospital Brno - International Clinical Research Center (FNUSA-ICRC)</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
International journal of obesity
ISSN
0307-0565
e-ISSN
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Volume of the periodical
40
Issue of the periodical within the volume
2
Country of publishing house
GB - UNITED KINGDOM
Number of pages
9
Pages from-to
266-274
UT code for WoS article
000369691500012
EID of the result in the Scopus database
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