Phospholipases D1 and D2 Suppress Appetite and Protect against Overweight
Please always quote using this URN: urn:nbn:de:bvb:20-opus-179729
- Obesity is a major risk factor predisposing to the development of peripheral insulin resistance and type 2 diabetes (T2D). Elevated food intake and/or decreased energy expenditure promotes body weight gain and acquisition of adipose tissue. Number of studies implicated phospholipase D (PLD) enzymes and their product, phosphatidic acid (PA), in regulation of signaling cascades controlling energy intake, energy dissipation and metabolic homeostasis. However, the impact of PLD enzymes on regulation of metabolism has not been directly determined soObesity is a major risk factor predisposing to the development of peripheral insulin resistance and type 2 diabetes (T2D). Elevated food intake and/or decreased energy expenditure promotes body weight gain and acquisition of adipose tissue. Number of studies implicated phospholipase D (PLD) enzymes and their product, phosphatidic acid (PA), in regulation of signaling cascades controlling energy intake, energy dissipation and metabolic homeostasis. However, the impact of PLD enzymes on regulation of metabolism has not been directly determined so far. In this study we utilized mice deficient for two major PLD isoforms, PLD1 and PLD2, to assess the impact of these enzymes on regulation of metabolic homeostasis. We showed that mice lacking PLD1 or PLD2 consume more food than corresponding control animals. Moreover, mice deficient for PLD2, but not PLD1, present reduced energy expenditure. In addition, deletion of either of the PLD enzymes resulted in development of elevated body weight and increased adipose tissue content in aged animals. Consistent with the fact that elevated content of adipose tissue predisposes to the development of hyperlipidemia and insulin resistance, characteristic for the pre-diabetic state, we observed that Pld1\(^{-/-}\) and Pld2\(^{-/-}\) mice present elevated free fatty acids (FFA) levels and are insulin as well as glucose intolerant. In conclusion, our data suggest that deficiency of PLD1 or PLD2 activity promotes development of overweight and diabetes.…
Author: | Jonathan Trujillo Viera, Rabih El-Merahbi, Bernhard Nieswandt, David Stegner, Grzegorz Sumara |
---|---|
URN: | urn:nbn:de:bvb:20-opus-179729 |
Document Type: | Journal article |
Faculties: | Fakultät für Biologie / Theodor-Boveri-Institut für Biowissenschaften |
Medizinische Fakultät / Institut für Experimentelle Biomedizin | |
Language: | English |
Parent Title (English): | PLoS ONE |
Year of Completion: | 2016 |
Volume: | 11 |
Issue: | 6 |
Article Number: | e0157607 |
Source: | PLoS ONE 2016, 11(6):e0157607. DOI:10.1371/journal.pone.0157607 |
DOI: | https://doi.org/10.1371/journal.pone.0157607 |
Dewey Decimal Classification: | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Tag: | adipose tissue; bioenergetics; body weight; enzyme regulation; hypothalamus; insulin; insulin resistance; mouse models |
Release Date: | 2020/12/11 |
Licence (German): | CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International |