Natural Dietary Products and Their Effects on Appetite Control

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Natural dietary products and their effects on appetite control Joon Hyuk Suh, Yu Wang, and Chi-Tang Ho J. Agric. Food Chem., Just Accepted Manuscript • DOI: 10.1021/acs.jafc.7b05104 • Publication Date (Web): 13 Dec 2017 Downloaded from http://pubs.acs.org on December 14, 2017

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Journal of Agricultural and Food Chemistry

Perspective Natural dietary products and their effects on appetite control Joon Hyuk Suh,† Yu Wang,†,* and Chi-Tang Ho§,* †

Food Science and Human Nutrition, Citrus Research and Education Center, University of Florida, 700 Experiment Station Rd, Lake Alfred, FL 33850 USA § Department of Food Science, Rutgers University, 65 Dudley Road, New Brunswick, NJ 08901, USA 8 9 10 11 12 13 14 15 16 17 18 19

Corresponding authors: Chi-Tang Ho, Tel: (848)-932-5553; Fax: (732)-932-6776; Email: [email protected] or Yu Wang, Tel: (863)-956-8673; Fax: (863)-956-4631; Email: [email protected];

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ACS Paragon Plus Environment

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Abstract

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Natural dietary products have been thoroughly studied for their effects of anti-

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adipogenesis to prevent and treat obesity for decades. Nevertheless, in the past few

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years appetite control for the treatment of obesity has attracted much attention as a new

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target. Homeostatic control of energy intake involves a complex system that conveys

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peripheral signals to the central nervous system where multiple signals are integrated

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and then provide feedback to regulate satiation. This perspective aims at elucidating the

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neuronal mechanisms of food intake and energy balance as well as providing an

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alternative pathway of controlling weight using natural dietary products.

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Keywords: natural dietary products, gut-related hormones, adiposity-related hormones,

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satiation, appetite control

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Introduction Obesity, excessive fat accumulation in the body, results in numerous associated

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metabolic diseases such as cardiovascular disease, type 2 diabetes, fatty liver disease

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and other pathological conditions.1 Obesity is on the rise worldwide, which has caused

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the World Health Organization (WHO) to declare being overweight as one of the top 10

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risk factors for disease.2 It has been projected that by 2030 more than one billion people

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will be affected. Global strategies for obesity focus on lifestyle and dietary modifications,

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including the restriction of energy intake and alteration of eating habits for either the

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prevention or delayed development of obesity.

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Appetite, which triggers food ingestion, is pivotal when studying obesity. Even the

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slightest difference of caloric intake over expenditure can cause weight gain, potentially

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leading to the development of obesity. There has been great progress in the research of

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the physiological mechanisms that regulate food intake and energy homeostasis.3

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Various gut and fat-derived neurotransmitters and hormones are involved in gut-brain

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communication, a physiological driver for appetite control, to relay information on the

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nutritional status of individuals to the central nervous system (CNS), more specifically,

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the hypothalamus and the brainstem.3 The hypothalamus is an important appetite-

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control center that integrates peripheral hormone signals and interacts with other brain

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regions to regulate food intake and satiation.

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The ideal anti-obesity treatments possess sustained clinical potency with minimal side effects. Due to drug safety concerns, there is an increasing demand in today’s


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market for natural products ubiquitous in edible plants. The estimated business potential

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for natural, cost-effective weight control products approaches two billion USD. Appetite-

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related neuropeptides and hormones are promising targets for obesity treatment. This is

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because these peptides tend to show higher receptor selectivity and have more

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receptor recognition sites.3 Some studies have indicated natural products as a potential

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candidate to treat obesity due to their ability to regulate food intake and energy

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homeostasis. For example, extracts from ginseng, green tea or grape seed are found to

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have anorexigenic effects by targeting multiple appetite-related neuropeptides and

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hormones.4-6 However, this is still a brand-new area for food chemistry research.

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Additional food resources that are regularly consumed should be studied. Furthermore,

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additional studies need to be completed to understand both the chemistry and

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mechanisms involved. In this perspective, we summarize the progress in understanding

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appetite regulation, including the peripheral and central pathways, as well as various

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neuropeptides and hormones. We also discuss natural dietary products as a promising

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material for appetite control.

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Peripheral appetite signals There have been numerous studies into the physiological mechanisms of appetite

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regulation in animal and human models. Results indicate more than 30 peripherally

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released hormones and neuropeptides that are now known to control appetite. The

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primary sources of appetite hormones are classified into adipocyte tissues and the

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gastrointestinal (GI) tract; the main secretion sites are the pancreas, stomach (antrum

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and fundus) and intestine (duodenum, jejunum and ileum).7 Ingested food drives gastric


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distension and hormone production from multiple sites in the gut, both of which can

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promote satiation and a desire to stop eating. Gut-brain communication, dubbed the

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gut-brain axis, is closely involved in the regulation of appetite. This communication

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appears to be bidirectional, signaling from the peripheral to the central nervous system

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(CNS) and from the central to the peripheral nervous system (PNS), mainly through the

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vagus nerves. The vagus nerves serve as mediator for appetite enhancing and

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suppression signals. The vagal afferent nerve located in the nodose ganglion is a

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bipolar neuron. One part (peripheral axon) is connected to peripheral organs, and the

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other (central axon) to the nucleus tractus solitarius (NTS), and projects to brain regions

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such as the brainstem and the hypothalamus, which both function to regulate food

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intake.7 Neuropeptides secreted from the digestive tract in response to dietary input

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could activate the vagal afferents by binding with their specific receptors at the vagus

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nerve terminals, which extend to mucosal layers of the GI tract.7 Electrical signals

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converted from gut peptide information reach the brain through the NTS, adjusting

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neurotransmitters and transporting signals to superior neurons toward the

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hypothalamus. The information is integrated in the hypothalamus in order to provide a

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regulating signal to the peripheral organs, including short term food ingestion and long

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term energy homeostasis. Central neuropeptides and hormones are also associated

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with this regulation mechanism. Fig. 1 shows the pathways of peripheral hormones

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modulating appetite centers in the brain.

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Gut-Related Hormone Signals


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Although there are various types of gut hormones, ghrelin released by gastric

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antrum and fundus is the only potent orexigenic peptide. Besides having growth

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hormone secretion activity, acylated ghrelin (5-20% of circulating ghrelin) plays a part in

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the short term food intake with a fundamental influence on appetite.8 The concentration

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of ghrelin rises during fasting while stimulating a desire to eat, and then gradually

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declines after meal ingestion. Ghrelin is expressed in not only the stomach but also the

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hypothalamus, acting as a neurotransmitter in the hypothalamic paraventricular area

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and arcuate nucleus. Central ghrelin along with ghrelin in peripheral areas could be

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sufficient and necessary to increase appetitive behaviors.9

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All other gut neuropeptides, such as glucagon-like peptide-1 (GLP-1), peptide YY

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(PYY) and cholecystokinin (CCK), work in the opposite manner as ghrelin.7 They have

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an anorectic effect that can induce satiation. These hormones are stimulated by nutrient

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intake, including carbohydrate, fat, and protein. Responding to the amount of

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carbohydrate and fat in a meal, both GLP-1 and PYY are co-secreted from the intestinal

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L cells that line the ileum and colon. The release of CCK produced by I cells located in

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the duodenum and jejunum follows the luminal nutrients, especially fat.7, 10 The

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circulating levels of GLP-1 increase postprandially and decrease while fasting. Although

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their half-life in plasma is just 1-2 min, leading to rapid inactivation after release, GLP-1

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has diverse roles; besides controlling appetite and energy intake, it acts as a strong

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incretin hormone that stimulates insulin secretion and inhibits glucagon secretion.11

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GLP-1 also retards gastric emptying, which reduces postprandial glycemia and

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enhances fullness after a meal.11 There has been some evidence indicating the


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relationship between appetite and GLP-1 levels; increased appetite was observed in

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obese subjects with lower fasting levels of GLP-1 after diet-induced short-term weight

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loss as compared to the same subjects after they slightly regained weight following a

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few months of dietary intervention.12 GLP-1 exerts its effects through activation of the

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GLP-1 receptors widely distributed in peripheral organs (GI tract and pancreas) and the

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brain (brainstem and hypothalamic nuclei).

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PYY exists in two endogenous forms, PYY1-36 and PYY3-36, which are

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postprandially released into the circulation. PYY3-36 is a major form having high binding

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affinity for the Y2 receptor among five G-protein coupled receptor subtypes (Y1, Y2, Y4,

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Y5, and Y6). PYY3-36 regulates food intake by stimulating Y2 receptors in the

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hypothalamic arcuate nucleus.13 Like GLP-1, PYY has an effect on delaying gastric

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emptying, which contributes to satiety and slows nutrient absorption. In addition, PYY

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has been reported to inhibit gastric, bile acid and pancreatic exocrine secretions, as well

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as regulate energy expenditure.13 Postprandial PYY levels have shown a positive

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correlation with the caloric value of the ingested meal, and following a meal, circulating

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levels of PYY peak within 2 h, remaining elevated for up to 6 hours.14

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CCK is secreted postprandially and distributed throughout both the GI tract and the

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CNS. There are multiple molecular forms of CCK, classified according to the number of

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amino acids (4 to 83 amino acids) they contain, for example, CCK-8, CCK-22, CCK-33,

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CCK-39 and CCK-58. The most abundant form in the brain is CCK-8, while the major

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circulating forms are CCK-22 and CCK-33. The function of CCK is diverse, including


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inhibition of gastric emptying, gallbladder contraction, gastric acid and pancreatic

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secretion, as well as suppression of food intake.7 Two types of receptors for CCK have

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been identified; CCK1 and CCK2 receptors. The anorexigenic effect of CCK seems to be

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mostly mediated by CCK1 receptors found in peripheral tissues, such as vagal afferent

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nerves.15 CCK1 receptors are also located in the brain, particularly in regions involved in

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the regulation of energy intake, including the NTS and the dorsal medial hypothalamus.

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The role of CCK2 receptors on appetite has been poorly investigated, but some studies

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suggest that hypothalamic CCK2 receptors may mediate inhibition of food ingestion and

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control satiety similar to the findings with the role of CCK1 receptors.15 Plasma CCK

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levels are increased by nutrient stimulation after a meal, rising about 15 min, and

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gradually decreasing within 5 h.16

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Adiposity-Related Hormone Signals Adiposity-related hormones including leptin and insulin influence long term energy

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balance in the body. Leptin is secreted from white adipose tissue (as well as the

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stomach) in proportion to total fat mass, and insulin released from pancreatic β-cells

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follows the ingestion of carbohydrates.7 Their circulating levels correlate with body

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adipose mass. Both leptin and insulin can be transported across the blood-brain barrier

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by using a saturable transporter, and access the hypothalamic neurons and other

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regions of the brain to regulate energy homeostasis. Leptin is implicated in several

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physiological effects such as feeding behavior and satiation by providing information of

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available energy resources to the brain.7 Its anorectic property is mainly controlled via

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arcuate nucleus, where centrally-projecting neurons express leptin receptors. The fact


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that decreased levels of leptin during starvation induce hunger reflects the role of leptin

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in appetite control. Leptin potentiates CCK signaling in vagal neurons, and they seem to

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act synergistically to reduce food ingestion and body weight.17 Although the circulating

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leptin levels imply the degree of adiposity, in the obese state, where leptin

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concentrations are high, there is some disorder of leptin’s ability to regulate energy

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balance, a phenomenon called leptin resistance.17 Larger amounts of leptin are required

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during this state to achieve the same effect when compared with normal individuals.

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Leptin resistance is supported by data indicating concentrations of leptin were found to

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be significantly higher in obese individuals than in the lean control individuals. Diet-

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induced weight loss has been reported to reduce fasting leptin levels and improve leptin

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sensitivity in human and animal studies.18

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Insulin is a well-known peptide hormone having effects on nutrient metabolism by

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increasing glucose uptake and inhibiting glucose production through signaling pathways

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in liver, muscle and fat. The role of insulin in the brain has been investigated in recent

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years. There has been growing evidence that insulin may regulate food intake and

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modulate food reward behaviors by triggering a signaling cascade in the brain.7 In

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addition, central insulin can affect glucose and fat homeostasis. While the mechanism of

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central insulin action has not been fully elucidated, the hypothalamus, especially

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paraventricular and arcuate nucleus regions, where insulin receptors are widely

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expressed, and the prefrontal cortex appears to be associated with its anorexic effects.

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Recently, the effects on appetite of intranasal insulin administration in fasting versus

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postprandial conditions in women has been investigated.19 Compared with placebo,


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appetite, as well as food intake were both found to decrease in the postprandial

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administration group but not the fasted group. This indicated that an anorexigenic effect

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of insulin might be amplified during the postprandial state. Obese individuals are prone

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to insulin resistance, similar to patients with type 2 diabetes. The relationship between

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weight gain and insulin resistance has been collected from a classical study in which

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lean subjects became insulin resistant through over-nutrition.20 High-fat feeding is

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revealed to disrupt insulin-signaling pathways in the brain, leading to hypothalamic

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inflammation and insulin resistance. Like leptin resistance, weight loss alleviates insulin

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resistance. There have been several studies investigating the effects of diet composition

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(e.g. low-fat vs low-carbohydrate diets) on weight loss. However, there were no

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significant effects detected for weight loss across diet groups, and fasting insulin levels

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declined significantly in insulin-resistance individuals. Recent evidence suggests that

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hypothalamic SIRT1, NAD+-dependent protein deacetylase, improves both leptin and

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insulin sensitivity by decreasing the concentrations of some molecules that deteriorate

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leptin and insulin signal transduction, bringing about the prevention of age-related

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weight gain.21

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Natural products and their effects on satiation

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There are not sufficient studies into natural dietary products and their effects on appetite

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control.5 Green tea has been shown to significantly improve insulin sensitivity and

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increase GLP-1 in patients with type 2 diabetes mellitus and lipid abnormalities.

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However, this study did not directly indicate the relationship of green tea consumption

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and appetite control. Although the major compound (-)-epigallocatechin-3-gallate


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(EGCG) in green tea was found to induce the secretion of CCK and GLP1 in an in vitro

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study using Caco-2 cells, the study employed only non-differentiated cells which might

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express low levels of proteins, i.e., functional transport proteins of enterocytes; therefore,

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further studies using differentiated cells are needed.22, 23 Grape seed proanthocyanidins

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can be used as a satiation agent by increasing the levels of GLP-1 in blood, with a

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decrease in gastric emptying.6 Ingestion of cinnamon can also delay gastric emptying

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rate and decrease postprandial feeling of hunger by adjusting insulin and GLP-1

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concentrations in healthy subjects, but the investigation of ingredients causing this

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effect in cinnamon remains to be elucidated.24 Capsaicin analog nonivamide from chili

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peppers was proven to increase GLP-1, leading to decrease in total energy intake from

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meal.25 β-Glucan, a soluble fiber from oats, was shown to significantly increase the level

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of plasma PYY in dose-dependent manner in overweight adults, implicating it can be

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used as an appetite suppressant.26 A recently published study showed chitosan derived

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from prawn shells can reduce feed intake in pigs by up-regulating growth hormone

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receptors and neuropeptide receptor 5 in the hypothalamus, as well as increase leptin in

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adipocytes, indicating the link between chitosan and appetite control.27 A lot of

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medicinal plants have been shown with a noteworthy anti-appetite effect. For example,

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celastrol extracted from the roots of Tripterygium Wilfordii was recently found to

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increase the sensitivity of the satiety hormone, leptin, leading to significant weight loss

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as well as suppression of food intake.28 Some saponins such as ginsenoside Rb1 in

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ginseng can inhibit food intake through modulating peripheral signals such as PYY, and

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leptin.4, 29 A steroid glycoside called H.g.-12 purified from Hoodia gordonii was

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demonstrated to activate a human bitter receptor, leading to induction of CCK release


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both in rat intestine (ex vivo) and in HuTu-80 cells (in vitro).30 However, these plants are

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used in traditional Chinese medicine and there are concerns regarding the toxicity of

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this plant. Therefore, additional dietary sources, particularly regularly consumed

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vegetables and fruits, need to be studied in order to discover positive, long-lasting

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appetite control in everyday life with the fewest side effects. In addition, for future

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studies, in vivo models are suggested instead of only in vitro models, because appetite

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control is a communication process between the gut and brain. In vitro models cannot

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deliver all the information in its entirety. However, in order to understand the chemistry,

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for example which compounds in the dietary products are the most effective, then in

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vitro models are a good option when performing bioactivity-guided fractionation and

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identification.


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30. Le Nevé, B.; Foltz, M.; Daniel, H.; Gouka, R., The steroid glycoside H.g.-12 from Hoodia gordonii activates the human bitter receptor TAS2R14 and induces CCK release from HuTu-80 cells. Am. J. Physiol. Gastrointest. Liver Physiol. 2010, 299, G1368-G1375.


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Figure Captions

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Figure 1. Gut- and adiposity-related hormones modulating appetite-regulating centers in the brain (yellow mark: anorexigenic, blue mark: orexigenic).


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Natural Dietary Products and Their Effects on Appetite Control

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