| 1. |
- Andersson, Per-Erik, et al.
(författare)
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Regression of left ventricular wall thickness during ACE-inhibitor treatment of essential hypertension is associated with an increase in insulin mediated skeletal muscle blood flow
- 1998
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Ingår i: Blood Pressure. - 0803-7051 .- 1651-1999. ; 7:2, s. 118-126
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Tidskriftsartikel (refereegranskat)abstract
- Left ventricular hypertrophy (LVH) has been associated with insulin resistance, a condition with an impaired insulin-mediated vasodilation in skeletal muscle. ACE-inhibitors have been reported to be superior to most other antihypertensive drugs in inducing a regression of LVH. In a double-blind study with parallel groups, 50 patients with essential hypertension were randomized to treatment with either fosinopril (20 mg o.d.) or atenolol (50 mg o.d.) for 12-16 weeks. Left ventricle wall thickness (LVWT, defined as the sum of interventricular septum and posterior wall), diastolic function (represented by the ratio between the E-wave and the A-wave of mitral blood flow) and femoral artery blood flow (FBF) were evaluated using ultrasonic measurements. FBF was measured at normoinsulinemia and after 2 h of euglycemic hyperinsulinemia. Before treatment, the insulin-induced increase in FBF was inversely related to the LVWT (r = -0.52, p < 0.02). The reduction in ambulatory 24-h SBP/DBP was 13/9 mmHg for fosinopril and 15/14 for atenolol, ambulatory DBP being significantly more reduced by atenolol (p = 0.03 for difference in treatment effect). However, only fosinopril treatment resulted in a significant reduction in LVWT (from 20.5 mm to 19.4 mm, p < 0.05). The degree of reduction in LVWT was related to the increase in FBF in the fosinopril group (r = -0.45, p < 0.05). For fosinopril (but not for atenolol), there was a positive relationship between the change in E/A ratio and the change in femoral artery stroke volume (r = 0.80, p < 0.01). Conclusion: Impaired insulin-induced stimulation of leg blood flow was related to an increased LVWT. Furthermore, during fosinopril treatment, regression of LVWT was associated with enhanced skeletal muscle blood flow during hyperinsulinemia. This indicates that impaired peripheral blood flow (and thereby increased afterload) may be a possible mechanism explaining the previously found association between insulin resistance and cardiovascular hypertrophy.
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| 2. |
- Carlstedt, F., et al.
(författare)
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Serum levels of parathyroid hormone are related to the mortality and severity of illness in patients in the emergency department
- 1997
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 27:12, s. 977-981
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Tidskriftsartikel (refereegranskat)abstract
- Hypocalcaemia is a common finding in intensive care patients. In addition, raised levels of parathyroid hormone (PTH) have been described. The explanation and clinical importance of these findings are yet to be revealed. To investigate the occurrence of hypocalcaemia and elevated PTH levels and their relationship to morality and the severity of disease, serum levels of PTH, ionized calcium (Ca2+) and the cytokines interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) were measured on arrival in the emergency department in a broad spectrum of 140 acutely ill patients patients suffering from common diseases such as stroke, acute abdominal disorders, obstructive lung diseases, heart failure, acute myocardial infarction, angina pectoris, trauma and infectious diseases. A score (APACHE II) was calculated to assess the severity of disease. Elevated PTH levels (> 55 pg ml-1) were seen in 16% of the patients, being most frequent in patients with myocardial infarction (28%) and congestive heart failure (42%). The levels were significantly correlated with the APACHE II score (r = 0.48, P < 0.0001) and with the length of stay in hospital (r = 0.26, P < 0.002). PTH was also significantly (P < 0.03) elevated in non-survivors compared with survivors and was found to be a stronger predictor of mortality (P < 0.01) than the APACHE II score (P < 0.02) in Cox's proportional hazard analysis. No close relationships were found between the cytokine levels and the indices of calcium metabolism. In conclusion, a rise in serum levels of PTH was common and related to the severity of disease and mortality in a mixed emergency department population.
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| 3. |
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| 4. |
- Edholm, David, et al.
(författare)
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Preoperative 4-week low-calorie diet reduces liver volume and intrahepatic fat, and facilitates laparoscopic gastric bypass in morbidly obese
- 2011
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Ingår i: Obesity Surgery. - : Springer Science and Business Media LLC. - 0960-8923 .- 1708-0428. ; 21:3, s. 345-350
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim of this study was to explore changes in liver volume and intrahepatic fat in morbidly obese patients during 4 weeks of low-calorie diet (LCD) before surgery and to investigate if these changes would facilitate the following laparoscopic gastric bypass.METHODS: Fifteen female patients (121.3 kg, BMI 42.9) were treated preoperatively in an open study with LCD (800-1,100 kcal/day) during 4 weeks. Liver volume and fat content were assessed by magnetic resonance imaging and spectroscopy before and after the LCD treatment.RESULTS: Liver appearance and the complexity of the surgery were scored at the operation. Eighteen control patients (114.4 kg, BMI 40.8), without LCD were scored similarly. Average weight loss in the LCD group was 7.5 kg, giving a mean weight of 113.9 kg at surgery. Liver volume decreased by 12% (p < 0.001) and intrahepatic fat by 40% (p < 0.001). According to the preoperative scoring, the size of the left liver lobe, sharpness of the liver edge, and exposure of the hiatal region were improved in the LCD group compared to the controls (all p < 0.05).CONCLUSIONS: The overall complexity of the surgery was perceived lower in the LCD group (p < 0.05), due to improved exposure and reduced psychological stress (both p < 0.05). Four weeks of preoperative LCD resulted in a significant decrease in liver volume and intrahepatic fat content, and facilitated the subsequent laparoscopic gastric bypass as scored by the surgeon
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| 5. |
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| 6. |
- Fugmann, Andreas, et al.
(författare)
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The effect of euglucaemic hyperinsulinaemia on forearm blood flow and glucose uptake in the human forearm
- 1998
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Ingår i: Acta Diabetologica. - : Springer Science and Business Media LLC. - 0940-5429 .- 1432-5233. ; 35:4, s. 203-206
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Tidskriftsartikel (refereegranskat)abstract
- Insulin-mediated stimulation of blood flow to skeletal muscle has been proposed to be of major importance for insulin-mediated glucose uptake. The aim of this study was to investigate the relative importance of blood flow and glucose extraction as determinants of insulin-mediated glucose uptake in the human forearm. Forearm blood flow (FBF), glucose extraction and oxygen consumption were evaluated for 100 min during the euglycaemic hyperinsulinaemic clamp (92 mU/l) in nine healthy subjects. FBF was measured by venous occlusion plethysmography. Forearm glucose uptake increased sevenfold during the hyperinsulinaemia (P<0.001). Forearm glucose extraction showed a minor increase during the first 10 min of hyperinsulinaemia, but the most marked increase took place between 10 and 20 min (+170%). Thereafter, only a minor further increase was seen. During the first 10 min of hyperinsulinaemia FBF was unchanged. Thereafter, FBF increased steadily to a plateau reached after 60 min (+50%, P<0.001). A close relationship between whole body glucose uptake and FBF was seen at the end of the clamp (r = 0.75, P<0.02), but at this time the relationship between whole body glucose uptake and forearm glucose extraction was not significant. The modest increase in O2 consumption seen at the beginning of the clamp (+19%) was not related to FBF during the early phase of the clamp. In conclusion, the early course of insulin-mediated glucose uptake in the human forearm was mainly due to an increase in glucose extraction. However, with time the insulin-mediated increase in blood flow increased in importance and after 100 min of hyperinsulinaemia FBF was the major determinant of glucose uptake.
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| 7. |
- Hedberg, Jakob, et al.
(författare)
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Increased plasma magnesium concentrations 3 years after biliopancreatic diversion with duodenal switch
- 2012
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Ingår i: Obesity Surgery. - : Springer Science and Business Media LLC. - 0960-8923 .- 1708-0428. ; 22:11, s. 1708-1713
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Tidskriftsartikel (refereegranskat)abstract
- Background Biliopancreatic diversion with duodenal switch, BPD-DS, is a surgical procedure for treatment of super obese patients. It renders very good weight results and it strongly reduces the incidence of type 2 diabetes. One important mechanism of weight reduction after BPD-DS is malabsorption. Hypomagnesemia is an established cardiovascular risk factor. While it is wellknown that magnesium levels decline after jejuno-ileal bypass and increase after gastric bypass surgery, information on how magnesium status is affected by BPDDS is scant. The aim of the present study was to evaluate plasma magnesium concentrations (P-Mg) after BPD-DS. Methods Thirty-one patients, all Caucasians (9 diabetics, 12 men, age 38±8 years, weight 159±22 kg, body mass index (BMI) 53.9±5.2 kg/m 2) underwent BPD-DS. We evaluated weight, glycated hemoglobin levels (HbA1c) and P-Mg preoperatively as well as at 1 and 3 years after surgery. All subjects were treated with vitamin and mineral substitution after surgery, including 100 mg of magnesium salt. P-Mg was analyzed with respect to changes over time, correlation to BMI and HbA1c levels before and 3 years after surgery. Results The plasma magnesium concentrations increased by 15 % from 0.77±0.07 to 0.88±0.09 mmol/l over 3 years (p <0.001). The weight loss was 71±25 kg. No patient had diabetes at follow-up. No correlations between P-Mg and BMI or HbA1c were seen. Conclusions Although exerting much of its weightreducing effect by a malabsorptive mechanism, BPD-DS yields a rise in P-Mg 3 years postoperatively, possibly contributing to the improved metabolic state after this operation.
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| 8. |
- Hänni, Arvo, et al.
(författare)
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Increased circulating magnesium concentrations after Roux-en-Y gastric bypass surgery in patients with type 2 diabetes
- 2018
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Ingår i: Surgery for Obesity and Related Diseases. - : Elsevier. - 1550-7289 .- 1878-7533. ; 14:5, s. 576-582
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Tidskriftsartikel (refereegranskat)abstract
- Background: Low circulating magnesium concentrations predict cardiovascular and all-cause mortality in patients with type 2 diabetes (T2D). Epidemiologic and clinical studies have indicated lower extra- and intracellular magnesium concentrations in patients with diabetes.Objective: We aimed to describe alterations, if any, in circulating magnesium concentrations after laparoscopic Roux-en-Y gastric bypass surgery (LRYGB) in patients with obesity and T2D.Setting: Outpatient clinic of obesity and central hospital.Methods: Retrospective analysis of 1-year outcome of plasma magnesium (p-Mg) and glucometabolic status in all consecutive patients who underwent primary LRYGBP and who completed the follow-up visits, including biochemical test panels 6 and 12 months after surgery.Results: LRYGBP and complete follow-up visits were performed in 51 patients with T2D and 86 patients without T2D. All patients were given similar dietary advice and multivitamin and mineral supplementation after surgery. Before RYGB, the patients with T2D showed lower p-Mg compared with patients without T2D (.79 ± .06 mM and .82 ± .05 mM, respectively, P<.01). P-Mg was inversely correlated to fasting blood glucose and glycosylated hemoglobin levels. After surgery, mean p-Mg increased by 5.2% in the group with T2D compared with 1.4% in the patients without T2D (P<.01), ending at an equal level of .83 mM. The alterations in p-Mg were inversely related to the changes in fasting glucose and glycosylated hemoglobin concentrations.Conclusion: The lowered p-Mg associated with impaired glucometabolic status in patients with T2D was increased after LRYGBP, reaching similar concentrations as in patients without T2D.
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| 9. |
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| 10. |
- Hänni, Arvo
(författare)
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Magnesium and the Insulin Resistance Syndrome
- 2001
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Insulin resistance, defined as a state of reduced insulin-mediated glucose uptake in peripheral tissues, and disorders such as obesity, hypertension, and dyslipidemia, have been found to be associated in the conglomerate of the insulin resistance syndrome. Some antihypertensive drugs have been shown to decrease insulin sensitivity further. In the studies described in this thesis relations between the magnesium status and some aspects of the insulin resistance syndrome were investigated. In a cross-sectional study serum Mg was found to be directly related to insulin sensitivity and lipoprotein lipase activity, and inversely to fasting glucose concentration. During treatment with angiotensin-converting enzyme inhibitors, ACEi, in patients with essential hypertension, an increase in serum Mg in relation to serum Ca was found to be correlated to improved insulin sensitivity and decreased serum lipid concentrations. In trials with ACEi or bendrofluazide treatment, a reduced Ca/Mg ratio in skeletal muscle was associated with the blood pressure response. A change in Mg concentration in skeletal muscle was inversely correlated to the change in serum glucose, but was not correlated to the insulin sensitivity per se. Atherogenic lipid fractions were more closely related to the plasma ionized Mg concentration than to circulating total Mg levels. Intra-arterial Mg infusion improved endothelium-dependent vasodilation, EDV, in healthy normotensive subjects. In summary, magnesium improves endothelium-dependent vasodilation and lipoprotein lipase activity, which might help to explain the inverse correlations between circulating Mg concentrations and some lipid and glucometabolic variables.The Mg content in skeletal muscle is related to blood pressure response and serum glucose levels during antihypertensive treatment with ACEi or bendrofluazide.
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