scholarly journals Impaired CNS Leptin Action Is Implicated in Depression Associated with Obesity

Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2634-2643 ◽  
Author(s):  
Nobuko Yamada ◽  
Goro Katsuura ◽  
Yukari Ochi ◽  
Ken Ebihara ◽  
Toru Kusakabe ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
High Fat Diet ◽  
Control Diet ◽  
Preference Test ◽  
Antidepressant Activity ◽  
Brain Derived Neurotrophic Factor ◽  
Epidemiological Studies ◽  
High Fat ◽  
Depressive Behavior ◽  
Sucrose Preference Test

Recent epidemiological studies indicate that obesity increases the incidence of depression. We examined the implication of leptin for obesity-associated depression. Leptin induced antidepressive behavior in normal mice in a forced swimming test (FST), and leptin-overexpressing transgenic mice with hyperleptinemia exhibited more antidepressive behavior in the FST than nontransgenic mice. In contrast, leptin-deficient ob/ob mice showed more severe depressive behavior in the FST than normal mice, and leptin administration substantially ameliorated this depressive behavior. Diet-induced obese (DIO) mice fed a high-fat diet showed more depressive behavior in the FST and in a sucrose preference test compared with mice fed a control diet (CD). In DIO mice, leptin induced neither antidepressive action nor increment of the number of c-Fos immunoreactive cells in the hippocampus. Diet substitution from high-fat diet to CD in DIO mice ameliorated the depressive behavior and restored leptin-induced antidepressive action. Brain-derived neurotrophic factor concentrations in the hippocampus were significantly lower in DIO mice than in CD mice. Leptin administration significantly increased hippocampal brain-derived neurotrophic factor concentrations in CD mice but not in DIO mice. The antidepressant activity of leptin in CD mice was significantly attenuated by treatment with K252a. These findings demonstrated that leptin induces an antidepressive state, and DIO mice, which exhibit severe depressive behavior, did not respond to leptin in both the FST and the biochemical changes in the hippocampus. Thus, depression associated with obesity is due, at least in part, to impaired leptin activity in the hippocampus.

scholarly journals Chronic administration of brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus reverses obesity induced by high-fat diet

2010 ◽  
Vol 298 (5) ◽  
pp. R1320-R1332 ◽  
Author(s):  
ChuanFeng Wang ◽  
Rebecca J. Godar ◽  
Charles J. Billington ◽  
Catherine M. Kotz
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
High Fat Diet ◽  
Control Diet ◽  
Brain Derived Neurotrophic Factor ◽  
Hypothalamic Paraventricular Nucleus ◽  
High Fat ◽  
Metabolic Indices

An acute injection of brain-derived neurotrophic factor (BDNF) in the hypothalamic paraventricular nucleus (PVN) reduces body weight by decreasing feeding and increasing energy expenditure (EE), in animals on standard laboratory chow. Animals have divergent responses to a high-fat diet (HFD) exposure, with some developing obesity and others remaining lean. In the current study, we tested two hypotheses: 1) BDNF in the PVN reverses HFD-induced obesity, and 2) animals with higher body fat have a greater physiological response to BDNF than those with less body fat. Eighty-four 10-wk old rats were allowed HFD ad libitum for 9 wk and then prepared with bilateral PVN cannulas. Animals were then divided into tertiles based on their body fat rank: high, intermediate, and low (H, I, and L). Each group was further divided into 2 subgroups and then PVN injected with BDNF or control (artificial cerebrospinal fluid, aCSF) every other day for 3 wk. Energy intake (EI), body weight, and body composition were measured. At study's end, rats were killed to allow measurement of other metabolic indices. In parallel, another 12 rats were fed control diet (CD), PVN-cannulated and injected with aCSF. HFD exposure induced obesity, particularly in the H body fat group, with a significant increase in EI, body weight, fat mass, liver size, and serum glucose, triglycerides, insulin, and leptin. BDNF significantly reduced EI, body weight, body fat, lean mass, and serum metabolic indices. These BDNF effects were greatest in the H body fat group. These data indicate that BDNF reduced HFD-induced obesity and metabolic syndrome-like measures, and the animals with the most body fat had the most significant response to BDNF.

Influence of a high-fat diet on brain-derived neurotrophic factor (BDNF)

Appetite ◽  
2008 ◽  
Vol 51 (2) ◽  
pp. 412
Author(s):  
N. Zeeni ◽  
C. Chaumontet ◽  
E. Moyse ◽  
N. Darcel ◽  
C. Tardivel ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
High Fat Diet ◽  
Brain Derived Neurotrophic Factor ◽  
High Fat

scholarly journals Curcumin evokes antidepressant-like effects in mice by regulating miR-124/brain derived neurotrophic factor

2021 ◽  
Vol 18 (3) ◽  
pp. 603-609
Author(s):  
Yanhong Yi ◽  
Jing Li ◽  
Weian Chen
Keyword(s):  
Neurotrophic Factor ◽  
Preference Test ◽  
Brain Derived Neurotrophic Factor ◽  
Mild Stress ◽  
Dependent Manner ◽  
Immobility Time ◽  
Swimming Test ◽  
Sucrose Preference Test ◽  
Loss Of Appetite

Purpose: To investigate the effect and mechanism of curcumin on depression in mice Methods: Mice were subjected to chronic unpredictable mild stress (CUMS), and behavioural changes were evaluated by sucrose preference test (SPT) and forced swimming test (FST). CUMS-treated mice received curcumin at a concentration of 50, 100, or 200 mg/kg. The level of MiR-124 was measured by real-time polymerase chain reaction (RT-PCR). Brain-derived neurotrophic factor (BDNF) levels were evaluated by western blotting. Results: CUMS induced depressive behaviour in mice, with increase in miR-124 and decrease in BDNF. Curcumin inhibited miR-124 expression and promoted BDNF in a dose-dependent manner in CUMS-treated mice. Brain-derived neurotrophic factor was the direct target of miR-124, decreasing the transcription of BDNF, but this was reversed by curcumin in vitro. MicroRNA-124 overexpression aggravated CUMS-induced depressive symptoms including loss of appetite, less sucrose consumption, shorter swimming time, and longer immobility time (p < 0.001). The effects were attenuated by curcumin. Conclusion: Curcumin alleviates CUMS-induced depressive behaviour by regulating miR-124/BDNF, suggesting that curcumin may a viable treatment option for depression.

Sign in / Sign up

Export Citation Format

Share Document