Brain-derived neurotrophic factor (BDNF) and type 2 diabetes
ABSTRACT Decreased levels of brain-derived neurotrophic factor (BDNF) have been implicated in the pathogenesis of Alzheimer's disease and depression. These disorders are associated with type 2 diabetes, and animal models suggest that BDNF plays a role in insulin resistance. We therefore explored whether BDNF plays a role in human glucose metabolism.
We included (Study 1) 233 humans divided into four groups depending on presence or absence of type 2 diabetes and presence or absence of obesity; and (Study 2) seven healthy volunteers who underwent both a hyperglycaemic and a hyperinsulinaemic-euglycaemic clamp.
Plasma levels of BDNF in Study 1 were decreased in humans with type 2 diabetes independently of obesity. Plasma BDNF was inversely associated with fasting plasma glucose, but not with insulin. No association was found between the BDNF G196A (Val66Met) polymorphism and diabetes or obesity. In Study 2 an output of BDNF from the human brain was detected at basal conditions. This output was inhibited when blood glucose levels were elevated. In contrast, when plasma insulin was increased while maintaining normal blood glucose, the cerebral output of BDNF was not inhibited, indicating that high levels of glucose, but not insulin, inhibit the output of BDNF from the human brain.
Low levels of BDNF accompany impaired glucose metabolism. Decreased BDNF may be a pathogenetic factor involved not only in dementia and depression, but also in type 2 diabetes, potentially explaining the clustering of these conditions in epidemiological studies.
Full-textDOI: · Available from: Christian Philip Philip Fischer, Aug 12, 2015
- SourceAvailable from: Serge Berthoin
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- "However, further investigation into this phenomenon needs to be completed before a substantive conclusion is made. Furthermore, these findings support the hypotheses that BDNF is linked to multiple parameters of energy metabolism and homeostasis in diabetes (Krabbe et al. 2007; Yamanaka et al. 2008). Nakagawa et al. (2002) injected BDNF subcutaneously into STZinduced diabetic mice with or without insulin administration. "
ABSTRACT: Exercise is known to have beneficial effects on cognitive function. This effect is greatly favored by an exercise-induced increase in neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1), especially with high-intensity exercises (HIE). As a complication of type 1 diabetes (T1D), a cognitive decline may occur, mostly ascribed to hypoglycaemia and chronic hyperglycaemia. Therefore, the purpose of this study was to examine the effects of acute HIE on cognitive function and neurotrophins in T1D and matched controls. Ten trained T1D (8 males, 2 females) participants and their matched (by age, sex, fitness level) controls were evaluated on 2 occasions after familiarization: a maximal test to exhaustion and an HIE bout (10 intervals of 60 s at 90% of their maximal wattage followed by 60 s at 50 W). Cognitive tests and analyses of serum BDNF, IGF-1, and free insulin were performed before and after HIE and following 30 min of recovery. At baseline, cognitive performance was better in the controls compared with the T1D participants (p < 0.05). After exercise, no significant differences in cognitive performance were detected. BDNF levels were significantly higher and IGF-1 levels were significantly lower in T1D compared with the control group (p < 0.05) at all time points. Exercise increased BDNF and IGF-1 levels in a comparable percentage in both groups (p < 0.05). In conclusion, although resting levels of serum BDNF and IGF-1 were altered by T1D, comparable increasing effects on BDNF and IGF-1 in T1D and healthy participants were found. Therefore, regularly repeating acute HIE could be a promising strategy for brain health in T1D. www.nrcresearchpress.com/doi/abs/10.1139/apnm-2014-0098Applied Physiology Nutrition and Metabolism 01/2015; 40(1). DOI:10.1139/apnm-2014-0098 · 2.23 Impact Factor
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- "that plasma levels of BDNF were decreased in participants with type 2 diabetes independent of obesity (Krabbe et al., 2007). Plasma BDNF was inversely associated with fasting plasma glucose, but not with insulin. "
ABSTRACT: Objective: The clinical relationship between brain-derived neurotrophic factor (BDNF) and cognitive function or mild cognitive impairment (MCI) is not well-understood. The purpose of this study was to identify the relationship between serum BDNF and cognitive function and MCI, and determine whether serum BDNF level might be a useful biomarker for assessing risk for MCI in older people. Materials and Methods: A total of 4463 individuals aged 65 years or older (mean age 72 years) participating in the study. We measured performance in a battery of neuropsychological and cognitive function tests; serum BDNF concentration. Results: Eight hundred twenty-seven participants (18.8%) had MCI. After adjustment for sex, age, education level, diabetes, and current smoking, serum BDNF was associated with poorer performance in the story memory, and digit symbol substitution task scores. Serum BDNF was marginally associated with the presence of MCI (odds ratio, 95% confidence interval: 1.41, 1.00–1.99) when BDNF was 1.5 SD lower than the mean value standardized for sex and age, education level, diabetes, and current smoking. Conclusion: Low serum BDNF was associated with lower cognitive test scores and MCI. Future prospective studies should establish the discriminative value of serum BDNF for the risk of MCI.Frontiers in Aging Neuroscience 04/2014; 6:69. DOI:10.3389/fnagi.2014.00069 · 2.84 Impact Factor
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- "Thus, the accelerated accumulation of visceral fat accompanied with prolonged sedentary behavior (Laye et al., 2006) may negatively affect a variety of signals that cross the bloodebrain-barrier and negatively affect brain structure and function. Finally, there is also some evidence to suggest that impaired glucose metabolism is associated with reduced central BDNF production (Krabbe et al., 2007). "
ABSTRACT: It is generally understood that regular moderate to vigorous physical activity (MVPA) promotes good health from head to toe. Evidence also supports the notion that too much sitting can increase all-cause mortality and risk of chronic diseases such as diabetes. Moreover, there is evidence that daily MVPA may not offset negative effects of sedentary behavior on systemic risk factors. We extend the discussion to brain structure and function and argue that while MVPA is recognized as a protective behavior against age-related dementia, sedentary behavior may also be an important contributor to brain health and even counteract the benefits of MVPA due to overlapping or interacting mechanistic pathways. Thus, the goals of this review are (1) to outline evidence linking both PA and sedentary behavior to neurobiological systems that are known to influence behavioral outcomes such as cognitive aging and (2) to propose productive areas of future research.Mental Health and Physical Activity 03/2014; 7(1). DOI:10.1016/j.mhpa.2014.01.001