Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

Громова, Л. В.; Fetissov, Sergueı̈ O.; Груздков, А. А.

doi:10.3390/nu13072474

Cited by 52 publications

(45 citation statements)

References 129 publications

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“…There is no data on the exact metabolic and absorptive capacity for d -galactose in individual segments of the rat small intestine and the assumption of saturated metabolic and absorptive capacity remains only hypothetical. Nevertheless, given the very large concentrations (0.55 M) administered and the fact that active transport of glucose (mediated by the same mechanism) becomes saturated at “high luminal concentrations” greater than 30 mM [ 44 ], we consider oversaturation highly plausible.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Acute Oral Galactose Administration on the Redox System of the Rat Small Intestine

et al. 2021

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Galactose is a ubiquitous monosaccharide with important yet incompletely understood nutritive and physiological roles. Chronic parenteral d-galactose administration is used for modeling aging-related pathophysiological processes in rodents due to its ability to induce oxidative stress (OS). Conversely, chronic oral d-galactose administration prevents and alleviates cognitive decline in a rat model of sporadic Alzheimer’s disease, indicating that galactose may exert beneficial health effects by acting in the gut. The present aim was to explore the acute time-response of intestinal redox homeostasis following oral administration of d-galactose. Male Wistar rats were euthanized at baseline (n = 6), 30 (n = 6), 60 (n = 6), and 120 (n = 6) minutes following orogastric administration of d-galactose (200 mg/kg). The overall reductive capacity, lipid peroxidation, the concentration of low-molecular-weight thiols (LMWT) and protein sulfhydryls (SH), the activity of Mn and Cu/Zn superoxide dismutases (SOD), reduced and oxidized fractions of nicotinamide adenine dinucleotide phosphates (NADPH/NADP), and the hydrogen peroxide dissociation rate were analyzed in duodenum and ileum. Acute oral administration of d-galactose increased the activity of SODs and decreased intestinal lipid peroxidation and nucleophilic substrates (LMWT, SH, NADPH), indicating activation of peroxidative damage defense pathways. The redox system of the small intestine can acutely tolerate even high luminal concentrations of galactose (0.55 M), and oral galactose treatment is associated with a reduction rather than the increment of the intestinal OS. The ability of oral d-galactose to modulate intestinal OS should be further explored in the context of intestinal barrier maintenance, and beneficial cognitive effects associated with long-term administration of low doses of d-galactose.

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Section: Discussionmentioning

confidence: 99%

The Effect of Acute Oral Galactose Administration on the Redox System of the Rat Small Intestine

et al. 2021

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“…SGLT1 and GLUT2 are major intestinal glucose transporters [ 31 ]. SGLT1 plays the dominant role in glucose absorption when glucose concentration is less than 30 mM, while GLUT2 makes the main contribution when glucose concentration is above 30 mM after food intake [ 3 ]. Translocation of GLUT2 from cytoplasm to BBM mediates massive glucose absorption, while internalization of GLUT2 from BBM to cytoplasm prevents postprandial hyperglycemia, which constitutes a dynamic balance [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

“…Luminal glucose is transported into epithelial cells through SGLT1 in the brush border membrane (BBM) and transported from intestinal epithelial cells to mesenteric vein through GLUT2 in the basolateral membrane (BLM) when the luminal concentration of glucose is lower than 30 mmol/L. However, with higher concentration of luminal glucose in postprandial condition, cytoplastic GLUT2 is translocated to BBM rapidly and transports glucose by facilitated diffusion, and thus, GLUT2-mediated glucose diffusion becomes the dominant approach of glucose absorption after meals [ 3 ]. Insulin and other hormones that promote secretion of insulin are upregulated; with increased blood glucose, insulin acts as a limiter of intestinal glucose absorption through internalizing GLUT2 from BBM to cytoplasm [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Berberine Decreases Intestinal GLUT2 Translocation and Reduces Intestinal Glucose Absorption in Mice

Zhang

Yang

et al. 2021

IJMS

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Postprandial hyperglycemia is an important causative factor of type 2 diabetes mellitus, and permanent localization of intestinal GLUT2 in the brush border membrane is an important reason of postprandial hyperglycemia. Berberine, a small molecule derived from Coptidis rhizome, has been found to be potent at lowering blood glucose, but how berberine lowers postprandial blood glucose is still elusive. Here, we investigated the effect of berberine on intestinal glucose transporter 2 (GLUT2) translocation and intestinal glucose absorption in type 2 diabetes mouse model. Type 2 diabetes was induced by feeding of a high-fat diet and injection of streptozotocin and diabetic mice were treated with berberine for 6 weeks. The effects of berberine on intestinal glucose transport and GLUT2 translocation were accessed in isolated intestines and intestinal epithelial cells (IEC-6), respectively. We found that berberine treatment improved glucose tolerance and systemic insulin sensitivity in diabetic mice. Furthermore, berberine decreased intestinal glucose transport and inhibited GLUT2 translocation from cytoplasm to brush border membrane in intestinal epithelial cells. Mechanistically, berberine inhibited intestinal insulin-like growth factor 1 (IGF-1R) phosphorylation and thus reduced localization of PLC-β2 in the membrane, leading to decreased GLUT2 translocation. These results suggest that berberine reduces intestinal glucose absorption through inhibiting IGF-1R-PLC-β2-GLUT2 signal pathway.

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“…There is no data on the exact metabolic and absorptive capacity for D-galactose in individual segments of the rat small intestine and the assumption of saturated metabolic and absorptive capacity remains only hypothetical. Nevertheless, given the very large concentrations (0.55 M) administered and the fact that active transport of glucose (mediated by the same mechanism) becomes saturated at "high luminal concentrations" greater than 30 mM glucose [51], we consider oversaturation highly plausible.…”

Section: Discussionmentioning

confidence: 99%

The effect of acute oral galactose administration on the redox system of the rat small intestine

Homolak

Perhoč

Knezović

et al. 2021

Preprint

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Galactose is a ubiquitous monosaccharide with important yet incompletely understood nutritive and physiological roles. Chronic parenteral D-galactose administration is used for modeling aging-related pathophysiological processes in rodents due to its ability to induce oxidative stress (OS). Conversely, chronic oral D-galactose administration prevents and alleviates cognitive decline in a rat model of sporadic Alzheimer’s disease indicating galactose may exert beneficial health effects by acting in the gut. The present aim was to explore acute time-response of intestinal redox homeostasis following oral administration of D-galactose. Male Wistar rats were euthanized at baseline (n=6), 30 (n=6), 60 (n=6), and 120 (n=6) minutes following orogastric administration of D-galactose (200 mg/kg). The overall reductive capacity, lipid peroxidation, the concentration of low molecular weight thiols (LMWT) and protein sulfhydryls (SH), the activity of Mn and Cu/Zn superoxide dismutases (SOD), reduced and oxidized fractions of nicotinamide adenine dinucleotide phosphates (NADPH/NADP), and hydrogen peroxide dissociation rate were analyzed in duodenum and ileum. Acute oral administration of D-galactose increased the activity of SODs and decreased intestinal lipid peroxidation and nucleophilic substrates (LMWT, SH, NADPH) indicating activation of peroxidative damage defense pathways. The redox system of the small intestine can acutely tolerate even high luminal concentrations of galactose (0.55 M) and oral galactose treatment is associated with a reduction rather than the increment of the intestinal OS. The ability of oral D-galactose to modulate intestinal OS should be further explored in the context of intestinal barrier maintenance, and beneficial cognitive effects associated with long-term administration of low doses of D-galactose.

show abstract

Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation

Cited by 52 publications

References 129 publications

The Effect of Acute Oral Galactose Administration on the Redox System of the Rat Small Intestine

The Effect of Acute Oral Galactose Administration on the Redox System of the Rat Small Intestine

Berberine Decreases Intestinal GLUT2 Translocation and Reduces Intestinal Glucose Absorption in Mice

The effect of acute oral galactose administration on the redox system of the rat small intestine

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