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- Bjornsson, E. S., et al.
(författare)
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Effects of hyperglycemia on interdigestive gastrointestinal motility in humans
- 1994
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Ingår i: Scand J Gastroenterol. - 0036-5521. ; 29:12, s. 1096-104
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Gastrointestinal motility disorders are common in patients with diabetes mellitus. Recent studies indicate that hyperglycemia can affect gastric emptying and gastric motility in healthy subjects and diabetics. METHODS: The effect of acute hyperglycemia on gastrointestinal motility was studied with a manometric technique in healthy subjects. Seven individuals, four men and three women, 23-34 years old, were studied on 2 different days. On 1 of the days a 5-h registration was performed after an overnight fast. On another day and after an initial basal period, acute steady-state hyperglycemia was induced by intravenous glucose infusion for 90 min. Motility variables were evaluated in four segments: in the gastric antrum, the proximal duodenum, the distal duodenum, and the proximal jejunum. RESULTS: Fasting migrating motor complex rhythm including migration of phase III prevailed during hyperglycemia. Compared with euglycemia, the motility index in phase II was lower during hyperglycemia in all segments studied. In the antrum the difference was 62% (p < 0.01); in the proximal duodenum, 37% (p < 0.01); in the distal duodenum, 44% (p < 0.05); and in the jejunum, 58% (p < 0.01). During hyperglycemia the prevalence of propagated contractions in phase II was significantly lower than during euglycemia both in the antrum and the proximal duodenum. In the last part of phase III in proximal duodenum most individual contractions were propagated in orad direction compared with early phase III, and this difference persisted during hyperglycemia. The number of long clusters was significantly increased during hyperglycemia as compared with euglycemia: 2.0 +/- 0.6 per hour versus 0.4 +/- 0.14 (p < 0.01). In late phase II plasma levels of motilin and pancreatic polypeptide were significantly decreased during hyperglycemia. CONCLUSION: Hyperglycemia not only reduces the motility in the stomach but also inhibits motility in both the duodenum and the jejunum. The results show that acute hyperglycemia has an important impact on small-intestinal motility.
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- Björnsson, Einar, 1958, et al.
(författare)
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Effects of insulin and beta-adrenergic blockade on the migrating motor complex in humans
- 1995
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Ingår i: Scand J Gastroenterol. - 0036-5521. ; 30:3, s. 219-24
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Interdigestive small-intestinal motility is suppressed by hyperglycemia and also by hyperinsulinemia per se. Since hyperinsulinemia may increase sympathetic activity, the present study was undertaken to ascertain to what extent insulin affects phase III of the migrating motor complex (MMC) and MMC-related duodenal retroperistalsis and whether beta-adrenergic receptors may mediate the effects of insulin. METHODS: Fasting motility was studied in eight healthy volunteers on three occasions with an eight-lumen perfused pressure catheter, with closely spaced recording points in the proximal duodenum. On the control day 5-h antroduodenojejunal manometry was performed. On another study day euglycemic hyperinsulinemic clamping was performed for 2 h after an initial basal recording. On a 3rd day motility was recorded during propranolol infusion, combined with a period of euglycemic hyperinsulinemia. RESULTS: During hyperinsulinemia complete absence of phase III of the MMC in the gastric antrum was observed, whereas 55% of the MMC had a gastric phase-III component on the control day. The duration of phase III in the proximal duodenum was decreased during hyperinsulinemia compared with the control period (p < 0.05). This inhibitory effect of insulin on the activity front was not prevented by beta blockade. Under control conditions the proportion of retroperistaltic pressure waves in the proximal duodenum was 13 +/- 8% in early phase III, increasing in late phase III to 79 +/- 15% (p < 0.01). Duodenal phase III during hyperinsulinemia showed a similar increase in retroperistalsis, from 4 +/- 4% in early phase III to 67 +/- 21% in late phase III (p < 0.01). The corresponding proportions during beta blockade were 16 +/- 10% and 86 +/- 14%, respectively. CONCLUSIONS: Hyperinsulinemia per se abolishes antral phase III and makes the duodenal phase III shorter but does not interrupt the distinct pattern of retroperistalsis in late phase III. Beta-adrenergic receptors seem not to be important for these effects of insulin or for the retroperistalsis in duodenal phase III.
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- Eliasson, Björn, 1959, et al.
(författare)
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Hyperinsulinaemia impairs gastrointestinal motility and slows carbohydrate absorption
- 1995
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Ingår i: Diabetologia. - 0012-186X. ; 38:1, s. 79-85
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Tidskriftsartikel (refereegranskat)abstract
- Experimental euglycaemic hyperinsulinaemia (insulin levels 46 +/- 4 mU/l) impaired the post-absorptive gastrointestinal motility in healthy individuals; the effect being particularly pronounced in the upper gastrointestinal tract (stomach and proximal duodenum). The postprandial gastric emptying, measured with a standardized 99mTc labelled meal, was also significantly delayed (t50 increased by 38% or 32 min). This was combined with a slower carbohydrate absorption (delay in peak blood glucose level about 40 min). Furthermore, during experimental hyperinsulinaemia higher blood glucose levels were seen at 120 min than at 60 min after food ingestion. This was not seen in any subject in the control study where only 0.9% NaCl was infused. Blood levels of the motility-stimulating hormone, motilin, were significantly lower during experimental hyperinsulinaemia. Thus, experimental hyperinsulinaemia impairs the gastrointestinal motility in both the postabsorptive and postprandial states. This effect is combined with a delayed carbohydrate absorption. Hyperinsulinaemia per se may thus lead to alterations in carbohydrate absorption and can also contribute to the gastrointestinal disturbances in diabetes.
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- Eliasson, Björn, 1959, et al.
(författare)
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Smoking cessation improves insulin sensitivity in healthy middle-aged men
- 1997
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Ingår i: Eur J Clin Invest. - 0014-2972. ; 27:5, s. 450-6
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Tidskriftsartikel (refereegranskat)abstract
- Cigarette smokers have recently been shown to exhibit insulin resistance, dyslipidaemia and markers of the insulin resistance syndrome (IRS). The aim of this study was to examine the effects of smoking cessation on insulin sensitivity and IRS. Forty male, non-obese healthy smokers participated in this open parallel study with 8 weeks of follow-up. Seventeen subjects were able to stop smoking, while 23 subjects continued to smoke and served as a controls group. Anthropometric and metabolic data were measured. Degree of insulin sensitivity was determined with the euglycaemic hyperinsulinaemic clamp technique. Smoking cessation increased insulin sensitivity and improved the lipoprotein profile in spite of a modest increase in body weight. Initial smoking habits correlated positively with the increase in BMI as well as the improvements in the metabolic variables after smoking cessation. These data support the view that smoking causes insulin resistance and IRS, and also demonstrate that the beneficial metabolic effects of smoking cessation override the effects of an accompanying modest increase in body weight.
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- Eliasson, Björn, 1959, et al.
(författare)
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The insulin resistance syndrome in smokers is related to smoking habits
- 1994
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Ingår i: Arterioscler Thromb. - 1049-8834. ; 14:12, s. 1946-50
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Tidskriftsartikel (refereegranskat)abstract
- The relationship between smoking habits, insulin resistance, and related risk factors for cardiovascular disease was examined in 57 middle-aged male smokers whose degree of insulin resistance was quantified by using the euglycemic clamp technique. Smoking habits correlated with degree of insulin resistance and consequently with various manifestations of the insulin resistance syndrome including levels of insulin, high-density lipoprotein cholesterol, triglycerides, and plasminogen activator inhibitor-1 (PAI-1) activity. Smoking habits, independent of degree of insulin resistance, were also related to levels of total cholesterol and low-density lipoprotein cholesterol as well as triglycerides. Stepwise regression analyses considering the effects of age, lean body mass, body fat, body mass index, waist/hip ratio, and alcohol consumption showed that only smoking habits and percent body fat were independently related to degree of insulin resistance. This study shows that insulin resistance and the insulin resistance syndrome are important but not unique contributors to the strong risk profile for cardiovascular disease in middle-aged men who smoke.
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- Smith, Ulf, 1943, et al.
(författare)
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Pathogenesis and treatment of diabetic vascular disease - illustrated by two cases
- 2006
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Ingår i: J Intern Med. - : Wiley. - 0954-6820. ; 260:5, s. 409-20
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Tidskriftsartikel (refereegranskat)abstract
- This publication is a summary of the presentations given at the First JIM Grand Round held at the Sahlgrenska University Hospital on 15 March 2006. The Grand Round was based on two case reports; a patient with type 2 diabetes and pronounced macrovascular disease and another patient with early microvascular disease combined with the macrovascular complications. The pathogenesis of the vascular complications and the current treatment regimens were discussed in relation to the history and examinations performed in these patients.
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