Leptin and insulin signaling in dopaminergic neurons: relationship between energy balance and reward system

Doan, Khanh V.; Choi, Yun Hee; Moh, Sang Hyun; Kinyua, Ann W.; Kim, Ki Woo

doi:10.3389/fpsyg.2014.00846

Cited by 59 publications

(41 citation statements)

References 113 publications

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“…Eating behavior is regulated by the homeostatic and hedonic systems of the brain . The hypothalamus plays a central role in maintaining the physiologic requirements of the body through regulatory neuropeptides such as leptin, ghrelin and orexin . Also, the regulation of eating behavior is involved with a reward system .…”

Section: Discussionmentioning

confidence: 99%

“…The majority of previous studies reported no significant correlation between DAT availability and body mass index (BMI), and the DAT was not thought to be involved in the neurobiology underlying obesity in humans . However, according to animal studies, insulin increases the levels and activity of DAT mRNA and, thereby, enhances the clearance of dopamine from the synapse …”

Section: Introductionmentioning

confidence: 99%

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Striatal dopamine transporter changes after glucose loading in humans

Pak

Seo

Kim

et al. 2019

Diabetes Obesity Metabolism

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Aims The dopamine transporter (DAT) actively translocates dopamine that is released from the presynaptic neurons across the membranes of nerve terminals into the extracellular space. We hypothesized that glucose loading‐induced changes in striatal DAT levels could be associated with food intake in humans. Materials and methods An intravenous bolus injection of 18F‐FP‐CIT was administered after infusion of glucose or placebo (normal saline), and emission data were acquired over 90 minutes in 33 healthy males. For a volume‐of‐interest‐based analysis, an atlas involving sub‐striatal regions of ventral striatum (VST), caudate nucleus and putamen was applied. DAT availability and binding potential (BPND) were measured using a simplified reference tissue method with cerebellum as the reference. Results The glucose‐loaded BPND from the VST negatively correlated with body mass index (BMI), whereas the placebo‐loaded BPND from the VST did not. After loading with glucose, there were substantial increases in BPNDs: 18.3%, 71.7% and 34.0% on average in the VST, caudate nucleus and putamen, respectively. Conclusion Striatal DAT changes after glucose loading, and BMI is associated with glucose‐loaded DAT availability, not with placebo‐loaded DAT availability. DAT might have a role in the reward system of eating behavior.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Striatal dopamine transporter changes after glucose loading in humans

Pak

Seo

Kim

et al. 2019

Diabetes Obesity Metabolism

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“…Leptin resistance could be the functional link between reward deficiency and persistent ingestive behavior. Leptin receptors are expressed on dopamine neurons in the ventral tegmental area 140 . As proven in rodents, leptin infusions into the ventral tegmental area inhibit the activity of dopamine neurons and decrease food intake 141 .…”

Section: The Hunter and Gatherer Lifestylementioning

confidence: 99%

The sedentary (r)evolution: Have we lost our metabolic flexibility?

Freese¹,

Klement²,

Ruiz-Núñez³

et al. 2017

F1000Res

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During the course of evolution, up until the agricultural revolution, environmental fluctuations forced the human species to develop a flexible metabolism in order to adapt its energy needs to various climate, seasonal and vegetation conditions. Metabolic flexibility safeguarded human survival independent of food availability. In modern times, humans switched their primal lifestyle towards a constant availability of energy-dense, yet often nutrient-deficient, foods, persistent psycho-emotional stressors and a lack of exercise. As a result, humans progressively gain metabolic disorders, such as the metabolic syndrome, type 2 diabetes, non-alcoholic fatty liver disease, certain types of cancer, cardiovascular disease and Alzheimer´s disease, wherever the sedentary lifestyle spreads in the world. For more than 2.5 million years, our capability to store fat for times of food shortage was an outstanding survival advantage. Nowadays, the same survival strategy in a completely altered surrounding is responsible for a constant accumulation of body fat. In this article, we argue that the metabolic epidemic is largely based on a deficit in metabolic flexibility. We hypothesize that the modern energetic inflexibility, typically displayed by symptoms of neuroglycopenia, can be reversed by re-cultivating suppressed metabolic programs, which became obsolete in an affluent environment, particularly the ability to easily switch to ketone body and fat oxidation. In a simplified model, the basic metabolic programs of humans’ primal hunter-gatherer lifestyle are opposed to the current sedentary lifestyle. Those metabolic programs, which are chronically neglected in modern surroundings, are identified and conclusions for the prevention of chronic metabolic diseases are drawn.

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“…Leptin through the 3-phosphoinositide pathway inhibits the apoptotic processes in neuronal cells and prevents the degradation of dopaminergic neurons caused by toxins [155,163]. Note that the dopaminergic neurons are involved in the effects of leptin on feeding behavior and energetic balance [164]. As a consequence, the decrease of leptin level and of activity of leptin system in the hypothalamus and other brain areas result in imbalance of neuronal interactions, abnormalities in the central regulation of peripheral metabolism, and insulin resistance, which leads to the metabolic, neuroendocrine and neurological disorders, including severe obesity, MS and T2DM [165].…”

Section: Leptin Signaling Systemmentioning

confidence: 99%

Brain Signaling Systems in the Type 2 Diabetes and Metabolic Syndrome: Promising Target to Treat and Prevent These Diseases

2015

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The changes in the brain signaling systems play an important role in etiology and pathogenesis of Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MS), being a possible cause of these diseases. Therefore, their restoration at the early stages of T2DM and MS can be regarded as a promising way to treat and prevent these diseases and their complications. The data on the functional state of the brain signaling systems regulated by insulin, IGF-1, leptin, dopamine, serotonin, melanocortins and glucagon-like peptide-1, in T2DM and MS, are analyzed. The pharmacological approaches to restoration of these systems and improvement of insulin sensitivity, energy expenditure, lipid metabolism, and to prevent diabetic complications are discussed.

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Leptin and insulin signaling in dopaminergic neurons: relationship between energy balance and reward system

Cited by 59 publications

References 113 publications

Striatal dopamine transporter changes after glucose loading in humans

Striatal dopamine transporter changes after glucose loading in humans

The sedentary (r)evolution: Have we lost our metabolic flexibility?

Brain Signaling Systems in the Type 2 Diabetes and Metabolic Syndrome: Promising Target to Treat and Prevent These Diseases

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