Neuronal control of energy homeostasis

Gao, Qian; Horváth, Tamas L.

doi:10.1016/j.febslet.2007.11.063

Cited by 122 publications

(97 citation statements)

References 179 publications

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“…The hypothalamus is known to be an important central area in the homeostatic control of feeding (28). In the current study, we did not observe any effects of treatment in the hypothalamus.…”

Section: Discussionsupporting

confidence: 47%

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

et al. 2015

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OBJECTIVEGlucagon-like peptide-1 receptor agonists (GLP-1RAs) are associated with reduced appetite and body weight. We investigated whether these effects could be mediated by the central nervous system (CNS). RESEARCH DESIGN AND METHODSWe performed a randomized crossover study in obese patients with type 2 diabetes (n = 20, mean age 59.3 6 4.1 years, mean BMI 32 6 4.7 kg/m 2 ), consisting of two periods of 12-week treatment with either liraglutide 1.8 mg or insulin glargine. Using functional MRI, we determined the effects of treatment on CNS responses to viewing food pictures in the fasted condition and 30 min after meal intake. RESULTSAfter 12 weeks, the decrease in HbA 1c was larger with liraglutide versus insulin glargine (D20.7% vs. 20.2%, P < 0.001). Body weight decreased during liraglutide versus insulin glargine (D23.3 kg vs. 0.8 kg, P < 0.001). After 10 days, patients treated with liraglutide, compared with insulin glargine, showed decreased responses to food pictures in insula and putamen (P £ 0.02). In addition, liraglutide enhanced the satiating effect of meal intake on responses in putamen and amygdala (P £ 0.05). Differences between liraglutide and insulin glargine were not observed after 12 weeks. CONCLUSIONSCompared with insulin, liraglutide decreased CNS activation significantly only after short-term treatment, suggesting that these effects of GLP-1RA on the CNS may contribute to the induction of weight loss, but not necessarily to its maintenance, in view of the absence of an effect of liraglutide on CNS activation in response to food pictures after longer-term treatment.Obesity and diabetes constitute a major health burden due to their pandemic occurrence (1) and their association with adverse consequences, such as cardiovascular disease (2). Obesity is the result of a long-term excess energy intake relative to expenditure, leading to increased weight and body fat mass. The central nervous system (CNS) has a major role in the regulation of food intake and the maintenance

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Section: Discussionsupporting

confidence: 47%

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

et al. 2015

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“…Sirkuit makan di hipothalamus bertanggung jawab dalam meregulasi perilaku makan (Gao et al, 2008;Sohn et al, 2013). Pada hypothalamic arcuate nucleus (ARC), terdapat dua kelompok neuron yang bekerja saling berlawanan dalam mempengaruhi perilaku makan.…”

Section: P E N D a H U L U A Nunclassified

“…Sebaliknya, kelompok neuron yang mengandung neuro-peptide Y (NPY) dan agouti-related peptide (AgRP) menyebabkan peningkatan perilaku makan. (Gao et al, 2008;Sohn et al, 2013).…”

Section: P E N D a H U L U A Nunclassified

PENGARUH PEMBERIAN EKSTRAK KULIT PISANG KEPOK KUNING (<em>Musa balbisiana</em>) TERHADAP ASUPAN MAKAN DAN BERAT BADAN TIKUS WISTAR (<em>Rattus norvegicus</em>) JANTAN

Fatchurohmah¹,

Meliala

2017

Scri. Biol.

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A B S T R A C TA positive energy imbalance results in overweight and obesity. Overweight and obesity are the major risk factors for many diseases, including diabetes, cardiovascular diseases, and mental health. Animal studies suggested that serotonin involves in food intake control. The Banana peel is a potential natural source of serotonin precursor; furthermore, it may influence food intake. This study aimed to determine the effect of banana peel extract on food intake and body weight gain in male Wistar rats. Twenty-four male Wistar rats (8-10 weeks old), were divided into four groups for feeding treatment. All four group were; the control group (C), the banana peel extract dosage of 4 g/kg BW group (T1), the banana peel extract dosage of 8 g/kg BW (T2), and the banana peel extract dosage of 16 g/kg BW (T3). The food intakes were measured daily, while rats body weights were recorded at the beginning and the end of the three days experimental periods. The study found the rats in the T1 group (8.80 ± 2.63) showed no significant difference in food intake compared to C group (10.68 ± 1.89), T2 group (6.65 ± 3.12), and T3 group (5.42 ± 1.59). Rats in the T2 group (p = 0.038) and T3 group (p = 0.005) showed lower food intake significantly compared to control group. After three days of treatment, the T3 group showed a significant decrease in body weight compared to control group (p = 0.008). This study concluded, the administration of banana peel extract dosage of 8 g/kg BW and 16 g/kg BW suppressed food intake, while the dosage of 16 g/kg BW reduced the body weight in male Wistar rats.KEY WORDS: food intake, banana peel, Wistar rat Penulis korespondensi: WIWIEK FATCHUROHMAH |

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“…Beginning with the 'glucostatic' and 'lipostatic' hypotheses, nutrients were considered strong candidates that could 'tell' the brain the state of satiety (glucose) or overall energy stores (fat), so that food intake and energy expenditure could be regulated to maintain energy balance. 1,2 Both of these hypotheses endure to this day. The lipostatic hypothesis remains as a central concept in our understanding of the regulation of energy balance.…”

mentioning

confidence: 99%

Peripheral satiety signals: view from the Chair

Sharkey

2009

Int J Obes

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The discovery and characterization of peripheral signals that regulate food intake and energy balance dates back over 50 years. Beginning with the 'glucostatic' and 'lipostatic' hypotheses, nutrients were considered strong candidates that could 'tell' the brain the state of satiety (glucose) or overall energy stores (fat), so that food intake and energy expenditure could be regulated to maintain energy balance. 1,2 Both of these hypotheses endure to this day. The lipostatic hypothesis remains as a central concept in our understanding of the regulation of energy balance. This is based on the key observations that (a) insulin is secreted from the pancreas in direct proportion to fat stores and provides a signal to the brain to initiate long-term changes in energy expenditure and food intake 3 and (b) the peptide hormone leptin is released from adipose tissue itself, and defects in either the production or the signalling of leptin lead to obesity. 4 The glucostatic hypothesis received validation with the discovery of glucose-sensitive neurons in the hypothalamic regions involved in the control of energy balance. 5,6 Over the years, other nutrient-based hypotheses were developed and the existing ones were modified, but none of these were completely capable of explaining the shortterm control of food intake or certain aspects of long-term energy balance. In the early 1970s, Gibbs et al. 7 found a gastrointestinal hormone, cholecystokinin (CCK), that produced satiety in rats. This discovery heralded the era of the 'gut hormones' as regulators of both food intake and energy balance. We now recognize more than 20 gut-derived peptides and lipid mediators are involved in aspects of energy homeostasis. [8][9][10] Many of these have now been tested or developed as potential therapeutic agents for the treatment of metabolic disorders or to aid in weight management. It seems unlikely that the full complement of peripheral energy balance signals have been discovered. As more are found, the opportunities for the development of novel therapeutics must be balanced with challenges of understanding their role in the physiology and pathophysiology of this complex regulatory system. Major challenges remain: How do the plethora of peripheral signals get integrated in the brain? Similarly, how does the brain actually receive these signals in the first place? In the three articles following this viewpoint, Timothy Moran, 11 Harvey Grill, 12 and Alastair Ferguson 13 and their colleagues begin to address these challenges by outlining where signals released from the gut and adipose tissues act to regulate energy balance.Peripheral signals arising from the gut are key elements in food intake regulation and energy balance, as discussed by Timothy Moran. 11 He illustrates how enteroendocrine peptides are released in sequence along the length of the gut and across the duration of a meal. These peptides regulate both the initiation of a meal and its termination. There are a multitude of anorexigenic peptide signals released from the gut. Moran ...

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Neuronal control of energy homeostasis

Cited by 122 publications

References 179 publications

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

PENGARUH PEMBERIAN EKSTRAK KULIT PISANG KEPOK KUNING (<em>Musa balbisiana</em>) TERHADAP ASUPAN MAKAN DAN BERAT BADAN TIKUS WISTAR (<em>Rattus norvegicus</em>) JANTAN

Peripheral satiety signals: view from the Chair

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