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Biomedical subjects

Kristian S Bjerve

Publications and source records attributed to Kristian S Bjerve.

7 recordsLinked to original sources
PubMed2006

Effects of n-3 fatty acids in subjects with type 2 diabetes: reduction of insulin sensitivity and time-dependent alteration from carbohydrate to fat oxidation.

BACKGROUND: Effects of fish oil supplements on metabolic variables are insufficiently clarified in type 2 diabetes. OBJECTIVE: We aimed to investigate short-term (1 wk) and longer-term (9 wk) effects of n-3 fatty acids. DESIGN: Twenty-six subjects with type 2 diabetes without hypertriacylglycerolemia participated in a double-blind controlled study. Median intake in the intervention group was 17.6 mL fish oil/d (1.8 g 20:5n-3, 3.0 g 22:6n-3, and 5.9 g total n-3 fatty acids). The control group received 17.8 mL corn oil/d (8.5 g 18:2n-6). RESULTS: Plasma phospholipid 20:5n-3 and 22:6n-3 increased, whereas 18:2n-6 decreased, in the fish oil group compared with the corn oil group after 1 wk. The two n-3 fatty acids also increased in adipose tissue biopsy samples taken after 9 wk in the fish oil group. Glucose concentrations (home-monitored) were approximately 1 mmol/L higher in the fish oil group than in the corn oil group at the end of the intervention (P = 0.035). Glucose utilization measured by using an isoglycemic clamp was lowered in the fish oil group compared with that in the corn oil group at the end of the intervention (P = 0.049), whereas glucagon-stimulated C-peptide tended to increase (P = 0.078). The fish oil group utilized less fat for oxidation after 1 wk, with a change to more fat and less carbohydrate oxidation after 9 wk (P = 0.040), than did the corn oil group. CONCLUSION: A high intake of fish oil moderately increases blood glucose and decreases insulin sensitivity in persons with type 2 diabetes without hypertriacylglycerolemia and alters carbohydrate and fat utilization in a time-dependent manner.

Adult↗
PubMed2003

Acute lowering of circulating fatty acids improves insulin secretion in a subset of type 2 diabetes subjects.

We tested the effects of acute perturbations of elevated fatty acids (FA) on insulin secretion in type 2 diabetes. Twenty-one type 2 diabetes subjects with hypertriglyceridemia (triacylglycerol >2.2 mmol/l) and 10 age-matched nondiabetic subjects participated. Glucose-stimulated insulin secretion was monitored during hyperglycemic clamps for 120 min. An infusion of Intralipid and heparin was added during minutes 60-120. In one of two tests, the subjects ingested 250 mg of Acipimox 60 min before the hyperglycemic clamp. A third test (also with Acipimox) was performed in 17 of the diabetic subjects after 3 days of a low-fat diet. Acipimox lowered FA levels and enhanced insulin sensitivity in nondiabetic and diabetic subjects alike. Acipimox administration failed to affect insulin secretion rates in nondiabetic subjects and in the group of diabetic subjects as a whole. However, in the diabetic subjects, Acipimox increased integrated insulin secretion rates during minutes 60-120 in the 50% having the lowest levels of hemoglobin A(1c) (379 +/- 34 vs. 326 +/- 30 pmol x kg(-1) x min(-1) without Acipimox, P < 0.05). A 3-day dietary intervention diminished energy from fat from 39 to 23% without affecting FA levels and without improving the insulin response during clamps. Elevated FA levels may tonically inhibit stimulated insulin secretion in a subset of type 2 diabetic subjects.

Adult↗
PubMed2002

[Lead poisoning--a case report].

Lead poisoning may cause irreversible health defects, including anaemia, central nervous system problems and various organ defects. We describe a patient with lead poisoning. A 54-year-old woman was admitted to hospital with anaemia and unspecific gastrointestinal symptoms. Peripheral blood smear and bone marrow aspirate showed basophilic stippling of erythrocytes suggestive of lead poisoning, which was confirmed by high concentrations of lead in her blood. The lead source was the glazing of a ceramic wine jug. Chelating therapy was started. Haemoglobin was normalised; the patient returned to work after nine months. Correct diagnosis and treatment can prevent serious health problems caused by lead poisoning.

Bone Marrow Examination↗
PubMed2002

[Lead poisoning--an overview].

MATERIAL AND METHODS: We present a review of the history, pathophysiology, diagnosis and treatment of lead poisoning based on relevant literature. RESULTS AND INTERPRETATION: The human body does not metabolize lead, and lead accumulation may cause organ failure. Lead poisoning may cause serious health defects, including anaemia, central nervous system problems and various organ defects. Sources of lead may be found in the home as well as in the workplace or elsewhere in our environment, but lead poisoning is an infrequent condition. Prevention is important, but manifest lead poisoning can be treated effectively.

Acute Disease↗
PubMed2002

High headache prevalence among women with hemochromatosis: the Nord-Trøndelag health study.

In this large cross-sectional population-based study, 51,272 persons responded to a headache questionnaire and were screened for hemochromatosis. Phenotypic hemochromatosis and the C282Y/C282Y genotype were both associated with an 80% increase in headache prevalence evident only among women. The reason for this association is unclear, but one may speculate that iron overload alters the threshold for triggering a headache by disturbing neuronal function.

Adult↗
PubMed2002

Hereditary hemochromatosis: the clinical significance of the S65C mutation.

Hereditary hemochromatosis (HH) is a common genetic disease with iron overload in certain organs, especially the liver. Most cases are homozygous for the C282Y mutation in the HFE gene; a few are C282Y heterozygous, compound C282Y/H63D heterozygous, or have no known mutation. A third mutation, S65C, has been associated with HH, but this finding is disputed. We have studied the clinical significance of various genotypes with the S65C mutation. In a population-based screening for HH in 65,238 persons, 613 had high serum transferrin saturation in two blood samples and were invited for HFE genotyping. In 556 persons with complete data sets, we studied the serum ferritin concentration and the risk of being diagnosed with phenotypic HH in the various genotypic groups. The phenotypic diagnosis was given without knowing the genotypic result. Except for the C282Y homozygotes, no differences in median serum ferritin concentrations were found between the various genotypic groups. However, the C282Y/S65C compound heterozygous group had a higher risk of being diagnosed with phenotypic HH than the wild-type group, as did the C282Y homozygous and the C282Y/H63D compound heterozygous groups. When combined with the C282Y mutation, the S65C mutation is associated with an increased risk of being diagnosed with phenotypic HH.

Amino Acid Substitution↗