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. 2018 Mar 20;17(1):55.
doi: 10.1186/s12944-018-0710-z.

Palmitoleic acid (16:1n7) increases oxygen consumption, fatty acid oxidation and ATP content in white adipocytes

Maysa M Cruz  1 , Andressa B Lopes  2 , Amanda R Crisma  3 , Roberta C C de Sá  1 , Wilson M T Kuwabara  3 , Rui Curi  3   4 , Paula B M de Andrade  4 , Maria I C Alonso-Vale  5
Affiliations

Palmitoleic acid (16:1n7) increases oxygen consumption, fatty acid oxidation and ATP content in white adipocytes

Maysa M Cruz et al. Lipids Health Dis. .

Abstract

Background: We have recently demonstrated that palmitoleic acid (16:1n7) increases lipolysis, glucose uptake and glucose utilization for energy production in white adipose cells. In the present study, we tested the hypothesis that palmitoleic acid modulates bioenergetic activity in white adipocytes.

Methods: For this, 3 T3-L1 pre-adipocytes were differentiated into mature adipocytes in the presence (or absence) of palmitic (16:0) or palmitoleic (16:1n7) acid at 100 or 200 μM. The following parameters were evaluated: lipolysis, lipogenesis, fatty acid (FA) oxidation, ATP content, oxygen consumption, mitochondrial mass, citrate synthase activity and protein content of mitochondrial oxidative phosphorylation (OXPHOS) complexes.

Results: Treatment with 16:1n7 during 9 days raised basal and isoproterenol-stimulated lipolysis, FA incorporation into triacylglycerol (TAG), FA oxidation, oxygen consumption, protein expression of subunits representing OXPHOS complex II, III, and V and intracellular ATP content. These effects were not observed in adipocytes treated with 16:0.

Conclusions: Palmitoleic acid, by concerted action on lipolysis, FA esterification, mitochondrial FA oxidation, oxygen consumption and ATP content, does enhance white adipocyte energy expenditure and may act as local hormone.

Keywords: Beta-oxidation; Bioenergetics; Lipogenesis; Lipolysis; Mitochondria; Triglyceride/fatty acid cycle.

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Figures

Fig. 1
Fig. 1
Basal (a) and isoproterenol-stimulated (b) lipolysis measuring by release of glycerol (nanomoles per 106 cells). c mRNA levels of Pnpla2 gene (arbitrary units). Experiments performed in differentiated 3 T3-L1 adipocytes treated for 9 days with vehicle, palmitic acid (16:0, 100 μM) or palmitoleic acid (16:1n7, 100 μM). Results are means ± SEM. * P < 0.05 16:1n7 vs. all groups. The results are the average of 3 independent experiments (n = 4/experiment)
Fig. 2
Fig. 2
a [1-14C]-palmitate incorporation into TAG (nanomoles of incorporated [1-14C]-palmitate per 106 cells) and b mRNA levels of aP2 (arbitrary units). Experiments performed in differentiated 3 T3-L1 adipocytes treated for 9 days with vehicle, palmitic acid (16:0, 100 μM) or palmitoleic acid (16:1n7, 100 μM). Results are means ± SEM. * P < 0.05 16:1n7 vs. all groups. The results are the average of 3 independent experiments (n = 6/experiment)
Fig. 3
Fig. 3
a Conversion of [1-14C]-palmitate into CO2 (nanomoles of converted [1-14C]-palmitate into CO2 per 106 cells) and b Free fatty acids released under lipolysis (μMol per liter per well). Experiments performed in 3 T3-L1 adipocytes under 9-days treatment with vehicle, etomoxir (40 μM), palmitic acid (16:0, 100 μM) or palmitoleic acid (16:1n7, 100 μM). Results are means ± SEM. * P < 0.05 vs. all groups. The results are the average of 3 independent experiments (n = 4/experiment)
Fig. 4
Fig. 4
Oxygen consumption by 3 T3-L1 adipocytes under (a) chronic (9 days) and b acute (24 h) treatments with vehicle, palmitic acid (16:0, 100 μM, respectively) or palmitoleic acid (16:1n7, 200 or 100 μM, respectively). Results expressed as percentage of control. Results are presented as means ± SEM. * P < 0.05 16:1n7 vs. all groups. The results are the average of 3 independent experiments (n = 6/experiment)
Fig. 5
Fig. 5
ATP content on 3 T3-L1 adipocytes under 9-day treatment with vehicle, etomoxir (40 μM), palmitic acid (16:0, 100 μM) or palmitoleic acid (16:1n7, 100 μM). Results expressed as percentage of control. Results are means ± SEM. * P < 0.05 16:1n7 vs. all groups. The results are the average of 3 independent experiments (n = 4/experiment)
Fig. 6
Fig. 6
Total content of subunits representing OXPHOS proteins complexes analyzed by western blot. a Complex I. b Complex II. c Complex III. d CoxIV. e Complex V. Experiments were performed in differentiated 3 T3-L1 adipocytes treated for 9 days with vehicle, palmitic acid (16:0, 100 μM) or palmitoleic acid (16:1n7, 100 μM). Results expressed as arbitrary units. Results are presented as means ± SEM. * P < 0.05 16:1n7 vs. all groups, # P < 0.05 16:1n7 vs. vehicle. The results are the average of 3 independent experiments (n = 4/experiment)
Fig. 7
Fig. 7
a Mitochondrial mass (percentage of florescence). b Citrate synthase activity (micromoles per minute per microgram of protein). Experiments performed in differentiated 3 T3-L1 adipocytes treated for 9 days with vehicle, palmitic acid (16:0, 100 μM) or palmitoleic acid (16:1n7, 100 μM). Results are means ± SEM. * P < 0.05 16:1n7 vs. all groups. The results are the average of 3–4 independent experiments (n = 6/experiment)
Fig. 8
Fig. 8
Treatment with 16:1n7 for 9 days stimulated both lipolysis (1) and FFA re-esterification (4) in 3 T3-L1 adipocytes. Raised lipolysis leads to FFA (2) and glycerol release. FFA follow different fates (3): re-esterification into TAG (4), plasma (5) and mitochondria oxidation (6). 16:1n7 raised mitochondrial parameters such as FAO (6), oxygen consumption (7) and ATP generation (8). In addition, ETC protein expression is also elevated by 16:n7: complex II (9), complex III (10) and ATP synthase (11). ATP augmentation contributes to reesterification (12). Altogether, 16:1n7 enhances WAT futile cycle (lipolysis-re-esterification cycle) as well as mitochondria bioenergetics
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