Moderate l-lactate administration suppresses adipose tissue macrophage M1 polarization to alleviate obesity-associated insulin resistance
Open accessAbstract
As a crucial metabolic intermediate, l-lactate is involved in redox balance, energy balance, and acid-base balance in organisms. Moderate exercise training transiently elevates plasma l-lactate levels and ameliorates obesity-associated type 2 diabetes. However, whether moderate l-lactate administration improves obesity-associated insulin resistance remains unclear. In this study, we defined 800 mg/kg/day as the dose of moderate l-lactate administration. In mice fed with a high-fat diet (HFD), moderate l-lactate administration for 12 weeks was shown to alleviate weight gain, fat accumulation, and insulin resistance. Along with the phenotype alterations, white adipose tissue thermogenesis was also found to be elevated in HFD-fed mice. Meanwhile, moderate l-lactate administration suppressed the infiltration and proinflammatory M1 polarization of adipose tissue macrophages (ATMs) in HFD-fed mice. Furthermore, l-lactate treatment suppressed the lipopolysaccharide-induced M1 polarization of bone marrow-derived macrophages (BMDMs). l-lactate can bind to the surface receptor GPR132, which typically drives the downstream cAMP-PKA signaling. As a nutrient sensor, AMP-activated protein kinase (AMPK) critically controls macrophage inflammatory signaling and phenotype. Thus, utilizing inhibitors of the kinases PKA and AMPK as well as siRNA against GPR132, we demonstrated that GPR132-PKA-AMPKα1 signaling mediated the suppression caused by l-lactate treatment on BMDM M1 polarization. Finally, l-lactate addition remarkably resisted the impairment of lipopolysaccharide-treated BMDM conditional media on adipocyte insulin sensitivity. In summary, moderate l-lactate administration suppresses ATM proinflammatory M1 polarization through activation of the GPR132-PKA-AMPKα1 signaling pathway to improve insulin resistance in HFD-fed mice, suggesting a new therapeutic and interventional approach to obesity-associated type 2 diabetes.
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Long-term lactate administration reduces adipose tissue inflammation and promotes thermogenesis.
“However, long-term lactate administration reduces adipose tissue inflammation and promotes thermogenesis [15, 16].”
From High-intensity interval training or lactate administration combined with aerobic training enhances visceral fat loss while promoting VMH neuroplasticity in female rats (2024) · cites this paper as [16]
The Abstract (page unavailable) reports that 12 weeks of moderate l-lactate administration suppressed proinflammatory adipose tissue macrophages and elevated white adipose tissue thermogenesis in high-fat-diet-fed mice. The claim captures both effects but omits the dose and mouse-model conditions, making it broader than the finding reported. (LLM, conf=0.82)
Experimental — accuracy not yet measuredEven without exercise, intravenous or oral lactate administration could relieve adipose tissue inflammation by GPR132-AMPKα1 pathway and promote adipocyte browning by GPR81-p38 MAPK pathway.
“Even when not engaged in exercise, intravenous or oral lactate administration could still relieve adipose tissue inflammation by G protein-coupled receptor 132 (GPR132)-AMPKα1 pathway and promote adipocyte browning by GPR81-p38 MAPK pathway [16, 54].”
From High-intensity interval training or lactate administration combined with aerobic training enhances visceral fat loss while promoting VMH neuroplasticity in female rats (2024) · cites this paper as [16]
The Abstract and Discussion (page numbers unavailable) report that lactate administration suppressed adipose-tissue macrophage inflammation through GPR132–PKA–AMPKα1 signaling in high-fat-diet-fed mice. The Experimental procedures specify intraperitoneal injections, not intravenous or oral administration. The Discussion mentions adipocyte browning in connection with PPARγ, but does not support the claimed GPR81–p38 MAPK browning pathway. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLactate administration without exercise could also promote catabolism of peripheral fat pads via the GPR132 pathway.
“a recent study found that lactate administration without exercise could also promote catabolism of peripheral fat pads via the GPR132 pathway [16].”
From High-intensity interval training or lactate administration combined with aerobic training enhances visceral fat loss while promoting VMH neuroplasticity in female rats (2024) · cites this paper as [16]
The Results (page not available in our copy) report that injected l-lactate reduced fat accumulation in high-fat-diet-fed mice and increased thermogenic markers in white adipose tissue. The Results and Discussion link GPR132 signaling to suppression of macrophage M1 polarization, not to catabolism of fat pads. The claimed GPR132 mechanism for fat-pad catabolism is therefore not established by this paper. (LLM, conf=0.86)
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- Authors
- Cai, H., Wang, X., Zhang, Z., Chen, J., Wang, F., Wang, L., & Liu, J.
- Affiliations
- Hefei University of Technology (CN)
- Corresponding author
- Liu, Jian
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2022-04
- Volume
- 298
- Issue
- 4
- Pages
- 101768
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC8941214
- OpenAlex
- W4213436587
- Cited by
- 60
- References
- 57
- Citations by year
- 2026: 13 · 2025: 17 · 2024: 14 · 2023: 15 · 2022: 1
- FWCI
- 8.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- L-lactate, adipose tissue macrophages, M1 macrophage polarization, obesity, insulin resistance, type 2 diabetes, GPR132, AMPK, cAMP/PKA signaling, high-fat diet, bone marrow-derived macrophages, lipopolysaccharide
- MeSH terms
- Adipose Tissue, Animals, Diabetes Mellitus, Type 2, Inflammation, Insulin Resistance, Macrophages, Obesity, Signal Transduction, Weight Gain, Lactic Acid, Mice, AMP-Activated Protein Kinases, Diet, High-Fat
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