| 1. |
- Jönsson, Anette, et al.
(författare)
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Long‑term follow‑up of buserelin‑induced enteric neuropathy in rats.
- 2016
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Ingår i: Molecular Medicine Reports. - : Spandidos Publications. - 1791-3004 .- 1791-2997. ; 13:4, s. 3507-3513
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Tidskriftsartikel (refereegranskat)abstract
- A few patients have been shown to develop severe abdominal pain and gastrointestinal dysmotility during treatment with gonadotropin‑releasing hormone (GnRH) analogs. A rat model of enteric neuropathy has been developed by administration of the GnRH analog buserelin to rats. Loss of enteric neurons and ganglioneuritis throughout the gastrointestinal tract has been described, without other histopathological changes. The aim of the present study was to investigate the long‑term effects of this rat model on body weight, and on morphology and inflammatory changes in the gastrointestinal tract. Rats were administered subcutaneous injections of buserelin or saline once daily for 5 days and allowed to recover for 3 weeks. This regimen was repeated four times. The rats were weighed weekly and were sacrificed 16 weeks after the fourth treatment. The bowel wall was measured by morphometry, and the presence of enteric neurons, mast cells, eosinophils and T‑lymphocytes was evaluated. Buserelin‑treated rats were shown to have a lower body weight at sacrifice, as compared with the controls (P<0.05). Compared with controls, buserelin treatment caused loss of myenteric neurons in the ileum and colon (P<0.01), a thinner circular muscle layer in ileum (P<0.05) and longitudinal muscle layer in colon (P<0.05), increased number of eosinophils in the submucosa of the ileum (P<0.05), and an increased number of T‑lymphocytes in the submucosa and circular muscle layer of the fundus (P<0.01 and P<0.05, respectively) and circular muscle layer of the colon (P<0.05). Mast cells were equally distributed in the two groups. Thus, long‑term follow‑up of buserelin‑induced enteric neuropathy reveals reduced body weight, loss of myenteric neurons, thinning of muscle layers, and increased numbers of eosinophils and T‑lymphocytes in the gastrointestinal tract.
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| 2. |
- Ohlsson, Bodil
(författare)
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Functional bowel symptoms in the general population (Review)
- 2022
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Ingår i: Molecular Medicine Reports. - : Spandidos Publications. - 1791-2997 .- 1791-3004. ; 26:1
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Forskningsöversikt (refereegranskat)abstract
- Several patients with irritable bowel syndrome (IBS) do not seek medical attention for their symptoms. When patients with IBS seek help, the majority of them are handled at primary healthcare centers, whereas research studies are performed at tertiary healthcare centers. The present study aimed to summarize findings from >4,000 participants of the general population included in the Malmö Offspring Study (inclusion rate 46.7%). The participants were clinically examined, their blood and fecal samples collected, and their questionnaires completed. The participants were divided into subjects with or without self?reported IBS and those having functional gastrointestinal (GI) symptoms in the past 2 weeks. The presence of IBS and GI symptoms in the participants were associated with each other. Zonulin levels did not differ between participants with or without GI diseases and were not associated with the degree of GI symptoms. The parameters low body weight at birth and small for gestational age were associated with the degree of the symptoms' influence on daily life. IBS and GI symptoms were positively associated with Blautia abundance. Beta?diversity differed between participants with or without these two conditions. Positive correlations were noted between the degree of diarrhea and the mean 24?h measurements of systolic blood pressure, diastolic blood pressure, and heart rate. Both IBS and GI symptoms were associated with female sex, smoking, stress, poor sleeping habits, unemployment, drug use, and a family history of GI diseases, whereas younger age was inversely associated with IBS and its associated symptoms. In conclusion, only a limited number of medical findings could be identified in participants with IBS and GI symptoms, whereas sociodemographic and environmental conditions were associated with these entities.
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| 3. |
- Ohlsson, Bodil
(författare)
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Theories behind the effect of starch‑ and sucrose‑reduced diets on gastrointestinal symptoms in irritable bowel syndrome (Review)
- 2021
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Ingår i: Molecular Medicine Reports. - : Spandidos Publications. - 1791-2997 .- 1791-3004. ; 24:4
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Forskningsöversikt (refereegranskat)abstract
- increased amounts of starch and sugar have been added to the diet in the Western world during the last decades. undigested carbohydrates lead to bacterial fermentation and gas production with diffusion of water, causing abdominal bloating, pain and diarrhea. Therefore, dietary advice is the first line of treatment of irritable bowel syndrome (IBS), a disease characterized by abdominal pain and altered bowel habits without any organic findings. recently, a diet with a reduction of starch and sucrose led to a marked effect on gastrointestinal (GI) symptoms. The mechanism is unknown, but three possible mechanisms are presented in the present review. First, functional variants of the enzyme sucrase‑isomaltase (SI) have been described in IBS. A subgroup of patients with IBS may thus suffer from partial SI deficiency with reduced digestion of starch and sucrose. Second, fructose absorption is less efficient than glucose absorption, which may lead to a physiological fructose malabsorption when ingesting high amounts of sucrose. a third mechanism is that high‑sugar diets causing hypergly‑ cemia, hyperinsulinemia and weight gain have led to painful neuropathy in animal models; whereas, improved metabolic control in humans has led to improvement of neuropathy. Starch‑ and sucrose‑reduced diets lead to decreased levels of c‑peptide, insulin, gastric inhibitory peptide, leptin and weight reduction. These metabolic changes may reduce the excitability of the hypersensitive nervous system often found in IBS and, thereby, lead to the reduced symptoms found after the diet. in conclusion, further studies are needed to investi‑ gate the pathophysiology behind development of symptoms after starch and sucrose intake, and the mechanisms behind symptom relief after reduced intake.
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