Low plasma lactate concentration as a biomarker of an incompetent brain-pull: A risk factor for weight gain in type 2 diabetes patients

Dyken, Regina van; Hubold, Christian; Meier, Sonja; Hitze, Britta; Marxsen, Aja; Oltmanns, Kerstin M.; Schweiger, Ulrich; Lehnert, Hendrik; Pellerin, Luc; Peters, Achim

doi:10.1016/j.psyneuen.2010.02.016

Cited by 4 publications

(3 citation statements)

References 41 publications

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“…In a recent population-based cohort study we could show that low fasting lactate concentrations were associated with long-term weight gain and increased postprandial hunger feelings in patients with type 2 diabetes mellitus [29]. These findings suggest that an inadequate cerebral lactate demand may contribute to weight gain.…”

Section: Discussionmentioning

confidence: 95%

Rise in Plasma Lactate Concentrations with Psychosocial Stress: A Possible Sign of Cerebral Energy Demand

Kubera¹,

Hubold²,

Otte³

et al. 2012

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Objective: It is known that exogenous lactate given as an i.v. energy infusion is able to counteract a neuroglycopenic state that developed during psychosocial stress. It is unknown, however, whether the brain under stressful conditions can induce a rise in plasma lactate to satisfy its increased needs during stress. Since lactate is i) an alternative cerebral energy substrate to glucose and ii) its plasmatic concentration is influenced by the sympathetic nervous system, the present study aimed at investigating whether plasma lactate concentrations increase with psychosocial stress in humans. Methods: 30 healthy young men participated in two sessions (stress induced by the Trier Social Stress Test and a non-stress control session). Blood samples were frequently taken to assess plasma lactate concentrations and stress hormone profiles. Results: Plasma lactate increased 47% during psychosocial stress (from 0.9 ± 0.05 to 1.4 ± 0.1 mmol/l; interaction time × stress intervention: F = 19.7, p < 0.001). This increase in lactate concentrations during stress was associated with an increase in epinephrine (R² = 0.221, p = 0.02) and ACTH concentrations (R² = 0.460, p < 0.001). Conclusion: Plasma lactate concentrations increase during acute psychosocial stress in humans. This finding suggests the existence of a demand mechanism that functions to allocate an additional source of energy from the body towards the brain, which we refer to as ‘cerebral lactate demand’.

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Section: Discussionmentioning

confidence: 95%

Rise in Plasma Lactate Concentrations with Psychosocial Stress: A Possible Sign of Cerebral Energy Demand

Kubera¹,

Hubold²,

Otte³

et al. 2012

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“…Ketone bodies have also been shown to affect food intake [13] and body weight gain [14]. From a clinical point of view, it has been suggested that both lactate [15] and ketone bodies [16] metabolism could play an important role in the development of obesity although the underlying mechanisms remain obscure.…”

Section: Introductionmentioning

confidence: 99%

Resistance to Diet-Induced Obesity and Associated Metabolic Perturbations in Haploinsufficient Monocarboxylate Transporter 1 Mice

et al. 2013

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The monocarboxylate transporter 1 (MCT1 or SLC16A1) is a carrier of short-chain fatty acids, ketone bodies, and lactate in several tissues. Genetically modified C57BL/6J mice were produced by targeted disruption of the mct1 gene in order to understand the role of this transporter in energy homeostasis. Null mutation was embryonically lethal, but MCT1 +/− mice developed normally. However, when fed high fat diet (HFD), MCT1 +/− mice displayed resistance to development of diet-induced obesity (24.8% lower body weight after 16 weeks of HFD), as well as less insulin resistance and no hepatic steatosis as compared to littermate MCT1 +/+ mice used as controls. Body composition analysis revealed that reduced weight gain in MCT1 +/− mice was due to decreased fat accumulation (50.0% less after 9 months of HFD) notably in liver and white adipose tissue. This phenotype was associated with reduced food intake under HFD (12.3% less over 10 weeks) and decreased intestinal energy absorption (9.6% higher stool energy content). Indirect calorimetry measurements showed ∼ 15% increase in O2 consumption and CO2 production during the resting phase, without any changes in physical activity. Determination of plasma concentrations for various metabolites and hormones did not reveal significant changes in lactate and ketone bodies levels between the two genotypes, but both insulin and leptin levels, which were elevated in MCT1 +/+ mice when fed HFD, were reduced in MCT1 +/− mice under HFD. Interestingly, the enhancement in expression of several genes involved in lipid metabolism in the liver of MCT1 +/+ mice under high fat diet was prevented in the liver of MCT1 +/− mice under the same diet, thus likely contributing to the observed phenotype. These findings uncover the critical role of MCT1 in the regulation of energy balance when animals are exposed to an obesogenic diet.

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“…Additionally, lactate is increasingly recognized as a supplementary fuel for injured brains, and exogenous lactate supplementation has been shown to alleviate symptoms of acute brain injury [ 58 ]. Moreover, the brain can utilize blood lactate as an energy source even under normal conditions, and any disruptions in lactate uptake or transport could further exacerbate the metabolic challenges faced by the brain in the context of diabetes [ 59 ].…”

Section: Discussionmentioning

confidence: 99%

Resistance training boosts lactate transporters and synaptic proteins in insulin-resistance mice

Bian,

Li,

Lou

2024

Heliyon

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Low plasma lactate concentration as a biomarker of an incompetent brain-pull: A risk factor for weight gain in type 2 diabetes patients

Cited by 4 publications

References 41 publications

Rise in Plasma Lactate Concentrations with Psychosocial Stress: A Possible Sign of Cerebral Energy Demand

Rise in Plasma Lactate Concentrations with Psychosocial Stress: A Possible Sign of Cerebral Energy Demand

Resistance to Diet-Induced Obesity and Associated Metabolic Perturbations in Haploinsufficient Monocarboxylate Transporter 1 Mice

Resistance training boosts lactate transporters and synaptic proteins in insulin-resistance mice

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