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Witek, K.;  Wydra, K.;  Filip, M. Hormonal and Neuronal Regulation of Sugar Intake. Encyclopedia. Available online: https://encyclopedia.pub/entry/25793 (accessed on 13 July 2025).
Witek K,  Wydra K,  Filip M. Hormonal and Neuronal Regulation of Sugar Intake. Encyclopedia. Available at: https://encyclopedia.pub/entry/25793. Accessed July 13, 2025.
Witek, Kacper, Karolina Wydra, Małgorzata Filip. "Hormonal and Neuronal Regulation of Sugar Intake" Encyclopedia, https://encyclopedia.pub/entry/25793 (accessed July 13, 2025).
Witek, K.,  Wydra, K., & Filip, M. (2022, August 03). Hormonal and Neuronal Regulation of Sugar Intake. In Encyclopedia. https://encyclopedia.pub/entry/25793
Witek, Kacper, et al. "Hormonal and Neuronal Regulation of Sugar Intake." Encyclopedia. Web. 03 August, 2022.
Hormonal and Neuronal Regulation of Sugar Intake
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This entry is adapted from the peer-reviewed paper 10.3390/nu14142940

Carbohydrates are important macronutrients in human and rodent diet patterns that play a key role in crucial metabolic pathways and provide the necessary energy for proper body functioning. Sugar homeostasis and intake require complex hormonal and nervous control to proper body energy balance. Added sugar in processed food results in metabolic, cardiovascular, and nervous disorders. The homeostasis of blood glucose or fructose levels requires strong interaction of not only the endocrine system (pancreatic hormones, stress hormones) but also communication of the nervous system. 

sugar carbohydrates sucrose glucose fructose high-sugar diet

1. Carbohydrate ADME Processes

The fate of carbohydrates in an organism can be described by the absorption, distribution, metabolism, and excretion (ADME) process. In mammals, dietary di-, oligo- and polysaccharides are digested in the mouth, stomach, and intestine and are broken down into monosaccharides by special (salivary amylase, stomach acid, and specific carbohydrases—glycoside hydrolases, respectively) enzymes, and finally, the small intestine absorbs them into the bloodstream. Cellulose dietary fibres are indigestible carbohydrates fermented in the large intestine using the presence of bacteria [1]. Monosaccharides are transported through the hepatic portal vein to the liver. Fructose and galactose are phosphorylated to glucose by fructo- and galactokinase. Glucose is metabolized in all body cells by glycolysis [2]. This metabolic pathway converts 1 glucose molecule into 2 pyruvic acid molecules—the substrate for the citric acid cycle (CAC). Glycolysis also releases 2 high-energy adenosine triphosphate (ATP) molecules and 2 molecules of reduced nicotinamide adenine dinucleotide. The complete breakdown of one glucose molecule by aerobic respiration (glycolysis + CAC) forms approximately 30–33 molecules of ATP [3]. Glucose serves as a substrate of cellular respiration or is stored as glycogen in glycogenesis [4].
Monosaccharides, including glucose and fructose, enter mammalian cells via two different types of membrane-associated carrier proteins: sodium-glucose linked transporters (SGLTs) and facilitated diffusion glucose transporters (GLUTs) [5][6][7]. SGLT and GLUT expression occurs in tissues (e.g., in the intestine, kidney, and liver) where energy requirements or sugar biotransformation is necessary for other metabolic pathways. Additionally, adult brain neurons are in high energy demand; therefore, transporter presence is found in the brain [8]. Neurons consume approximately 20% of glucose-derived energy, making them the main consumer of glucose. Glucose enters the mammalian brain from the blood across the blood–brain barrier (BBB), which galactose and fructose are believed to cross. The large blood-brain concentration gradient drives the facilitating transport of glucose across endothelial membranes via GLUT1 glucose transporters into the extracellular fluid. GLUT1 further mediates glucose uptake from the extracellular fluid into astrocytes, oligodendroglia, and microglia, whereas GLUT3, which has a much higher transport rate than GLUT1, facilitates neuronal glucose uptake [9]. The expression of GLUT1 is much higher than that of GLUT3 in the developing and prenatal brain. In neurons and astrocytes, glucose is the source of pyruvate to fuel the citric acid cycle for the production of ATP. The SGLTs that mediate secondary active transport are likely not active in healthy conditions but rather in pathologic situations [10]. In contrast to glucose (80–120 mg/dL) [11][12], circulating levels of fructose in blood plasma are extremely low (<0.050 mM) [13][14]. The process of transporting fructose from the blood to the brain is unclear, and the data collected remain inconclusive.
The most important organ regulating carbohydrate metabolism in mammals is the liver. Here, the control of energy homeostasis is mainly reduced to regulation of the level of glucose in the blood. Glucose delivered to hepatocytes leads to de novo lipogenesis (DNL), the synthesis of lipids (glycogen) stored in complex particles—lipoproteins in the liver. The decrease in glucose levels during starvation leads to the breakdown of glycogen stores or the synthesis of glucose as a result of gluconeogenesis [15]. Epidemiological studies have indicated that diets rich in simple sugars increase both DNL and the growth of peripheral, subcutaneous, and internal adipose tissue [16]. Below, several factors, including pancreatic hormones, diet, and the body’s energy balance, are discussed in the context of their roles in the conversion of glucose into lipids and lipids into glucose.

2. Pancreatic Hormones Control Blood Glucose Homeostasis

The glucoregulation process is responsible for maintaining a constant level of glucose in the body [17]. Hormones released from pancreatic cells play an important role in this negative feedback regulation, and their release is controlled by the amount of glucose present [18]. When blood glucose levels drop, leading to hypoglycaemia, pancreatic alpha cells are activated, and glucagon is released. Glucagon is transported with the blood, e.g., to the liver, where it activates glucagon receptors, enhances the process of glycogenolysis and inhibits glycogenesis. Glycogenolysis breaks down spare glycogen into glucose and releases it into the bloodstream. During hyperglycaemia (i.e., an increase in glucose levels in the blood), insulin, another pancreatic hormone, is released. Similar to glucagon, insulin is transported with the blood to the liver but enhances the process of glycogenesis and accelerates the uptake of glucose from the blood by muscle and adipose tissue cells [19][20][21].

3. Sweetness Perception and Regulation

The processing of sweet taste information is related to the presence of taste receptor cells (TRCs) expressing G-protein coupled receptors (GPCRs) concentrated in the taste buds of the tongue [22]. The taste 1 receptor family and the taste 2 receptor family of type 2 TRC receptor cells are capable of detecting sweet tastes. Upon activation with a sweet molecule ligand, the GPCR receptor activates the chemosensing signalling pathway [23]. Finally, ATP is released by the semichannels, activates the purinergic receptors present on the afferent fibres of the cranial nerves of the taste buds, and sends signals to the brain taste perception areas located in the gustatory cortex [24]. In the intestines, sweet taste receptors are concentrated mainly on enteroendocrine cells that secrete bioactive molecules, e.g., hormones. Sweet taste receptors in the gastrointestinal tract are responsible for nutrient detection, glucose homeostasis, and the secretion of gastrointestinal peptides [25]. The taste information from the intestines via the vagus nerve moves to the rostral division of the nucleus of the tractus solitarius (in rodents also to the parabrachial nucleus) and then to the parvicellular part of the ventral posteromedial nucleus of the thalamus, via the ventral path to the amygdala and to lateral areas of the hypothalamus [26][27].

4. Energy-Balanced Peptide Hormones

Sugar intake and metabolism are controlled by peptide hormones, such as leptin and ghrelin. Leptin is produced by adipocytes, whereas ghrelin is secreted by gastric enteroendocrine cells [28][29]. Leptin and ghrelin, together with blood, penetrate the BBB and regulate the activity of the hypothalamic melanocortin system in the area of the arcuate nucleus (ARC) [30]. One group of ARC neurons—anorexigenic—expresses the precursor peptide pro-opiomelanocortin (POMC) and CART (cocaine and amphetamine-regulated transcript). POMC is converted into α-melanocyte-stimulating hormone (α-MSH) and serves as a melanocortin 4 receptor (MC4R) agonist. Activation of POMC/CART neurons by leptin causes anorexic effects, including reduced food intake, weight loss, the release of α-MSH, and decreased release of NPY. The second group of neurons–orexigenic–expresses neuropeptide Y (NPY) and the MC4R antagonist agouti-associated protein (AgRP). Activation of NPY/AGRP neurons by ghrelin causes increased food consumption, weight gain, AgRP release, and decreased α-MSH release [31][32]. Leptin induces weight loss by suppressing food intake, whereas ghrelin acts as an appetite stimulant signal. A high-sugar diet (HSD) (rich in carbohydrates) causes an increase in leptin concentrations and a decrease in circulating ghrelin levels, which are greater than with a high-fat diet (HFD) [33].

5. Stress-Induced Bingeing “Comfort Food”

As discussed above, exposure to several stressors alters the metabolic and behavioural status of the body [34]. Stress factors activate feedback interactions along the hypothalamic–pituitary–adrenal (HPA) axis. The response to stress is release of the peptide corticotropin-releasing hormone (CRH) in the paraventricular nucleus of the hypothalamus. CRH is transferred through the hypothalamo-hypophyseal portal system to the anterior pituitary gland and stimulates corticotrophic cells to release adrenocorticotropic hormone (ACTH) from POMC. Via the bloodstream, ACTH travels to the adrenal glands, where it stimulates the secretion of cortisol, which is the most important stress-induced hormone [35][36]. Cortisol regulates glucose and lipid metabolism, appetite, food consumption, and weight gain [37][38]. Exposure to stress (prenatal and postnatal) can alter both the amount and the quality of calories consumed, and stress-induced changes in food consumption and energy balance can interact with the emotional state of humans [39][40]. The high reactivity of cortisol to stress can increase susceptibility in humans to eating palatable products rich in fat or sugar, called “comfort food” [41][42][43][44][45]. Similar to clinical observations, enhancement of palatable food intake has been reported in rodents during stress. Experimental animals choose “comfort food” to reduce depression and/or anxiety status [43][46]. As demonstrated in the limited sucrose intake paradigm, sucrose solution reduced stress responses [47][48][49]. Consumption of sucrose or highly sweet foods can limit activation of the stress system by an effect on the reward circuits in the brain [50][51]. Conversely, enhanced sugar intake can promote stress-driven emotional and addictive behaviours [52][53].

6. Changes in the Reward Brain System Following HSD

The reward brain system (the mesocorticolimbic pathway) is based on brain structures and neural pathways related to rewards, motivation, and the desire for pleasure [54][55]. The reward system contains numerous interrelated structures, such as the ventral tegmental area, nucleus accumbens (NAc), prefrontal cortex (PFC), hippocampus, and amygdala [56][57]. In humans, excessive consumption of glucose or fructose predisposed individuals to changes in activity in areas of the brain known to be associated with reward, learning reward, and eating behaviour. The fructose effect was limited to the activity of neurons, whereas glucose had a wide impact on the brain [58][59][60]. A diet high in sugar, including glucose, may cause excessive distribution of glucose to the brain [61], contributing to behavioural changes in food intake [62].
Recent preclinical data indicate that excessive sugar intake changed the reward circuitry at neurochemical and cellular levels as well as developed addictive-like behaviours and emotional states [63][64][65][66][67][68][69]. The changes depended on sugar dietary patterns. Thus, at the neurochemical level intermittent access to sucrose enhanced the dopaminergic, opioid and cholinergic neurotransmission in the mesocorticolimbic system [70][71]. Binge-like sugar consumption facilitated dopamine (DA) release in the NAc, similarly to drugs of abuse [72]. Long-term consumption of sucrose altered nicotinic acetylcholine receptor (nAChR) expression in the NAc, whereas nAChR compounds evoked different effects on sucrose intake depending on its long-term vs. short-term exposure [73][74]. Sucrose solution given chronically (7 or 21 days) to male rats increased the level of accumbal DA neurotransmission [71][72][75]. Additionally, a 25% glucose solution over 31 days increased the expression of accumbal D1 and μ-opioid receptors in female rats [76]. Finally, a maternal HSD changed the MC4R expression in brain reward structures in male and female offspring [77][78][79].
Moreover, at the cellular levels a binge-like sucrose intake by rats for long-term (12 weeks) period, but not for short-term (4 weeks) period, resulted in alterations within the medium spiny neurons in the NAc shell (but not core) with a significant reduction in dendritic length and increased distal dendritic spine density [80]. Sucrose served as a potent modulator of neuron morphology following prolonged heavy use, as its consumption enhanced excitatory synaptic strength onto NAc DA neurons [74]. In addition to sucrose, previous studies have demonstrated similarities following acute exposure to another non-caloric sweetener saccharin at the level of the NAc [81][82][83]. A very recent study indicated that chronic (12 weeks) 5% sucrose consumption to mice resulted in a reduction in the serotonin (5-HT) receptors innervation within the PFC and dentate gyrus of the hippocampus, a reduction in the number of microglia in the latter brain structure as well as a decrease in the density of the vesicular glutamate transporter (VGLUT3) and of 5-HT/VGUT3 varicosities but not in the number of oligodendrocyte progenitor cells [84].

7. Behavioural Consequences of HSD

In humans, HSD let to memory impairment and cognitive deficits [85][86], whereas it does not increase the improvement of semantic memory [87]. An observational study in children indicated that sucrose consumption was associated with the incidence of impulsivity and attention deficit hyperactivity disorder (ADHD) among 6-year-old boys and that persistent, high consumption or an increase in sugar consumption between 6 and 11 years of age was not associated with a higher prevalence of ADHD between 6 and 11 years of age [88].
Preclinical research reported that a higher (25%) but not low (5%) sucrose concentration given for a long time (12 weeks) to adolescent mice resulted in enhancement of hyperlocomotor response to novelty and defects in episodic and spatial memory in adulthood without modulation of learning processes [89]. In rodents, an HSD had a negative impact on aspects of behavioural tasks involving decision making and behaviour selection. A 2 h intake of sucrose over a 24-day period induced a significant spatial memory deficit as measured by site recognition in rats. Moreover, rats entering the delay discounting task had behavioural evidence of hippocampal dysfunction [90]. Hippocampus-dependent alteration in behaviours was accompanied with altered hippocampal neurogenesis such as a reduction in the proliferation and differentiation of newborn neurons in the dentate gyrus [89], which raises a positive correlation between high- and long-term exposure to sucrose during adolescent and neurocognitive defects in adulthood. Furthermore, anxiety-like or depressive-like symptoms being observed simultaneously following long-term 8–25% sucrose consumption [70][91][92][93][94][95][96][97], but not with 5% sucrose consumption [84]. In addition, a high sucrose intake (30% wt/vol) in pregnant mice induced behavioural phenotypes similar to ADHD in the offspring, manifested by increased motor activity, and impulsivity. As well as, high fructose consumption (30% wt/vol) induced hyperactive behaviour, similar to the results obtained with sucrose treatment [98]. These findings suggest that the maternal HSD (sucrose or fructose) consumption could be considered a potential new risk factor in neurobehavioural dysregulation, such as the development of ADHD and/or possibly addiction-like behaviours.

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Subjects: Nutrition & Dietetics
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Kacper Witek
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Karolina Wydra
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Małgorzata Filip
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Update Date: 04 Aug 2022
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