Chinese researchers from the Hefei University of Technology have found that a particular type of dietary flavonoid called luteolin has a significant effect on energy expenditure in mice, by helping to minimise excess fat storage, a major risk factor for type 2 diabetes, cardiovascular disease, and hypertension.
The study findings, published in the International Journal of Obesity, show that luteolin activates adipose (fat) browning – the process of recruiting brown fat cells – and thermogenesis, two co-dependent processes that boost fat burning and dissipate energy as heat.
Previous experiments conducted at Hefei’s department of Biological Sciences and School of Biotechnology and Food Engineering had evidenced that luteolin could improve diet-induced obesity and insulin resistance in mice.
Another dysfunction which lies at the core of obesity and associated metabolic disorders like type 2 diabetes is excess energy stored as fat in white adipose tissue (WAT). The developmental and functional induction of brown adipose tissue (BAT), however, promotes metabolic health.
There was no clear explanation for the occurrence of such a phenomenon until this study, which demonstrated that dietary luteolin regulates browning and thermogenesis via a recently uncovered metabolic pathway known as AMP-activated protein kinase (AMPK)/PGC1 alpha signalling.
Upon exploring the development, regulation and function of healthful BAT cells or thermogenic adipocytes, the research team established a link between the activity in BAT and WAT and AMPK/PGC1 alpha-mediated hypothalamic circuits, which could be somewhat regulated by dietary intake of luteolin.
In order to estimate the action of luteolin in fat tissues, the research scientists looked at changes in the energy expenditure of mice fed either a low-fat diet (LFD) without luteolin supplementation (constituting the control group) or high-fat diet (HFD) supplemented with 0.01% luteolin.
In another independent study, even-aged mice (to rule out the effects of ageing on metabolic rate) received a low-fat diet as well as luteolin-containing LFD.
After 12 weeks, the animals’ energy expenditure as well as intra-cellular molecular regulators, such as AMPK, were assessed in adipose tissues using a calorimetry system.
Regardless of the mice’s diet, dietary luteolin supplementation enhanced energy expenditure by upregulating thermogenic genes in BAT. At the same time, the AMPK/PGC1 alpha pathway was directly activated by luteolin in the tissues.
At a molecular level, the brown fat function that can counteract obesity was enabled by the activation of AMPK (resulting from the spike of luteolin in tissues) through the PGC1 alpha receptors located in the tissues.
Other studies have hypothetised that this process is mediated by a key uncoupling protein exclusively expressed in BAT called UCP1 and which is responsible for preventing metabolic dysfunction in mice.
This suggests that increasing the activity of BAT could be considered a therapeutic option for human obesity and may be facilitated by luteolin supplementation. Good amounts of luteolin can be obtained from foods like thyme (51.00mg per 100g), parsley (19.75mg per 100g), or peppermint (11.33mg per 100g) and to a lesser extent in pepper, rosemary and lemon.

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