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K D Palitzsch

Publications and source records attributed to K D Palitzsch.

At least 19 recordsLinked to original sources
PubMed2004

[Newly diagnosed diabetes mellitus--what to look out for].

Screening for diabetes makes good sense in particular in patients with overweight, hypertension or dyslipidemia. For type 2 diabetes is often not recognized until sequelae have put in an appearance. Consideration must be given to the possible presence of neuropathy, micro- and macroangiopathy and cardiovascular and cerebral disease. The primary therapy recommendations for type 2 diabetics comprise diet, weight loss and increased exercise. Depending on the success of these measures and the patient's constitution, medication with biguanides, sulfonylureas, glinides, glitazones alpha-glucosidase inhibitors or, where indicated, insulin, is then applied.

Adolescent↗
PubMed2002

The Pro115Gln polymorphism within the PPAR gamma2 gene has no epidemiological impact on morbid obesity.

The peroxisome-proliferator-activated receptor gamma2 (PPAR gamma2) is a transcriptional key regulator of adipocyte differentiation. PPAR gamma2 can be inactivated by phosphorylation of a serine residue at position 114. A point mutation leading to an amino acid exchange at position 115 (Pro115Gln) was shown to preclude serine phosphorylation and to consecutively accelerate adipocyte differentiation emphasizing the pathophysiological relevance of this mutation. So far, four markedly obese heterozygote carriers of the Pro115Gln mutation (body mass index 37.9-47.3 kgxm (-2)) have been identified in a circumscribed study population. In order to evaluate the epidemiological relevance of the Pro115Gln mutation in morbid obesity we screened the DNA of all subjects with a body mass index greater than 35 kgxm (-2) who had participated in a nationwide German epidemiological field survey. There was no homozygote or heterozygote carrier of the Pro115Gln polymorphism among them. We conclude that the Pro115Gln polymorphism within the PPAR gamma2 gene has no relevant epidemiological impact on morbid obesity in Germany. It needs further investigation whether this polymorphism might play a role in related metabolic disorders.

Adult↗
PubMed2001

Intracellular depletion of insulin by oleate is due to an inhibited synthesis and not to an increased secretion.

In the polyclonal rat pancreatic beta-cell line INS-1, immunoreactive insulin (IRI, insulin and its precursors) and C-peptide (surrogate marker for mature insulin) were quantified after a 1-h incubation at 16.7 mM glucose with or without oleate. Oleate caused a 20% decrease (P <or= 0.01) and a shift towards mature insulin (P <or= 0.01) in intracellular IRI. As IRI secretion was significantly (P <or= 0.01) diminished in the presence of oleate at hyperglycemic conditions the loss of intracellular IRI had to be due to other reasons which was then examined by focussing on newly synthesized, radiolabelled IRI*. Thereby, oleate caused a 50% decrease in newly synthesized intracellular IRI* (P <or= 0.01) and-contrary to the findings in complete intracellular IRI-a shift towards immature insulin precursors. Taken together, exposure of INS-1 cells to oleate induces an intracellular lack of uncompletely processed IRI. This is due to an inhibited biosynthetic supply which can not compensate for intracellular IRI-degradation and (to a neglible extent) for insulin secretion.

Animals↗
PubMed2001

GG-genotype in the promotor region of uncoupling-protein-1 gene is associated with lower level of dehydroepiandrosterone in type 2 diabetes.

The A-->G (-3826) point mutation within the distal region of the uncoupling-protein-1 (UCP-1) promoter is possibly involved in the development of obesity, diabetes and related disorders. DHEAS has been found to stimulate expression of UCP-1-mRNA. The aim of our study was to evaluate the prevalence of the three UCP-1 genotypes in type 2 diabetic patients out of a population based sample. Possible associations of A-->G mutation with serum levels of DHEAS and with obesity, diabetes and retinopathy were examined. - In 549 diabetic patients (312 males and 237 females) out of a population-based sample UCP-1 genotype was determined by genomic PCR and Bcl-I-RFLP analysis. Serum levels of DHEAS were measured by ELISA. - Genotype frequencies were: GG genotype, 4.4% (n= 24); AG genotype 37.3% (n=205) and AA genotype 58.3% (n= 320). The genotype groups were comparable with respect to sex, BMI, HbA1c, systolic blood pressure (BP), retinopathy and also to serum levels of C-peptide, leptin and cortisol. Serum levels of DHEAS were lowest in GG-genotype as compared to AG and AA (GG: 1.8+/-1.5 micromol/l, AG: 2.2+/-1.8 micromol/l, AA: 2.6+/-2.1 micromol/l; AA vs AG, AA vs GG: p<0.05). In a multiple linear regression analysis, which controlled for age, C-peptide, cholesterol, systolic BP, BMI, and HbA1c DHEAS was significantly negatively correlated with levels of cholesterol and positively with systolic BP only in females (p<0.05). - Allelic frequency for G in diabetic subjects was 0.23 which was similar as compared to a non-diabetic population examined by us in an earlier study. GG-genotype was associated with low levels of DHEAS in diabetic patients but not with retinopathy. We suggest a role for UCP-1 polymorphism in the pathogenesis of obesity and arteriosclerosis. This hypothesis, however, needs further investigation.

Aged↗
PubMed2001

Successful treatment of erectile dysfunction and infertility by venesection in a patient with primary haemochromatosis.

A 36-year-old patient with primary haemochromatosis presented with erectile dysfunction. Laboratory findings revealed reduced levels of luteinizing hormone (0.4 IU/l; normal range 2-12 IU/l), follicle-stimulating hormone (0.1 IU/l; normal range 1-12 IU/l) and testosterone (0.49 microg/l; normal range 2-8.1 microg/l). We made the diagnosis of secondary hypogonadism due to haemochromatosis, which is generally supposed to be irreversible. Due to consequent venesection therapy, levels of ferritin and transferrin saturation could be normalized, and levels of luteinizing hormone and follicle-stimulating hormone increased to normal ranges. Also, testosterone levels became normal and remained so without any androgen substitution. The patient subsequently regained erectile function and potency. This case underlines the fact that a hypogonadotrophic hypogonadism caused by iron overload can be reversed by a consequent venesection therapy.

Adult↗
PubMed2001

Frequency and significance of Pro12Ala and Pro115Gln polymorphism in gene for peroxisome proliferation-activated receptor-gamma regarding metabolic parameters in a Caucasian cohort.

Peroxisome proliferation-activated receptor-gamma2 (PPARgamma2) is exclusively expressed in adipose tissue and belongs to the transcriptional regulators of adipocyte differentiation. Recently, two missense single-point mutations have been described in the PPARgamma2 gene: Pro12Ala and Pro115Gln. It was our aim to determine the frequency of these polymorphisms in a Caucasian cohort and to investigate their possible role in the pathogenesis of obesity, type 2 diabetes, and related metabolic disorders. The genotypes of 359 subjects (149 males, 210 females) with varying degrees of obesity and with or without type 2 diabetes were determined. Subsequent to genomic polymerase chain reaction amplification, the HpaII restriction fragment length polymorphism (RFLP) analysis and the HindII RFLP analysis were used for genotyping the Pro12Ala and Pro115Gln polymorphism, respectively. For the Pro115Gln polymorphism, all 359 subjects showed wild-type sequence, emphasizing the very rare occurrence of the mutated allele. For the Pro12Ala polymorphism, 276 subjects (76.9%) were homozygous for the wild-type allele, 80 (22.3%) were heterozygous, and only 3 (0.8%) were homozygous for the mutated allele. Genotype frequency was calculated to be 0.88 for the wild-type allele and 0.012 for the mutated allele. No significant differences were found in age; gender; body mass index; total cholesterol; low-density, high-density, and very low density lipoproteins; triglycerides; Lp(a); uric acid; and diabetes manifestation by comparing the different genotypes. Therefore, a major role of these polymorphisms in the pathogenesis of obesity and diabetes can be excluded.

Adult↗
PubMed2001

Prevalence of markers of hepatitis B in the adult German population.

The prevalence of hepatitis B virus markers was investigated in 5305 individuals considered to be representative for the adult German population. After adjustment of the data according to the age and sex distribution in the whole German population an anti-HBc prevalence of 8.71% (95% confidence interval, 7.94-9.48%) and an HBsAg carrier rate of 0.62% (95% confidence interval, 0.40-0.84%) were calculated. Anti-HBc prevalence increased with age from 4.12% in the youngest group to 15.66% in the 61-70-year-old. The percentage of HBsAg carriers showed a maximum of 1.12% in the 41-50-year-old individuals and decreased significantly in the older age groups. 1.40% (95% confidence interval, 1.08-1.72%) of individuals had anti-HBc only. There was a trend to higher rates of this pattern in males than in females; a significantly higher percentage of persons with anti-HBc only was found in anti-HBc-positive individuals below 31 years than in older individuals. Five participants with anti-HBc only (7.7%, or about 0.1% of the whole population) showed HBV-DNA despite the absence of HBsAg. 3.1% of anti-HBc positive individuals where also positive for anti-HCV, that was significantly higher than the percentage of anti-HCV-positives among persons without any HBV marker (0.46%). This study provides a comprehensive picture of the current hepatitis B situation in Germany, showing new data especially on the distribution of HBsAg in the general population and on the subgroup of individuals with anti-HBc only.

Adolescent↗
PubMed2000

[Diabetic retinopathy and associated risk factors in type-1 and type-2 diabetics in the Upper Palatinate].

BACKGROUND AND OBJECTIVE: Diabetic retinopathy is the main cause of blindness in industrial countries. This study was undertaken to determine the prevalence of diabetic retinopathy and risk indicators among volunteers in a rural district in Bavaria, Germany. PATIENTS AND METHODS: Using a mobile survey unit, we investigated 627 diabetic volunteers (275 women, 352 men, mean age 64.5 +/- 12.5 yr) in 23 cities and villages. One retinal Polaroid photo was taken per eye, using a non-mydriatic camera (Canon CR4-45 NM). RESULTS: In 60 subjects (9.6%) retinal photographs were not assessable. Among the remaining 567 patients (76 type-1 diabetes, HbA1c 7.3 +/- 1.2% and 491 type-2 diabetes, HbA1c 7.7 +/- 1.5%) in 72.3% no retinopathy was found (57.9% type-1 diabetes/74.5% type-2 diabetes). Non-proliferative retinopathy was diagnosed in 22% (38.2%/19.6) and proliferative retinopathy in 5.6% (3.9%/5.9%). Photocoagulation scars were present in 6.1% (11.7%/5.3%) and macular oedema in 11.8% (14.1%/11.6%). In 6.1% (5.3%/6.6%) of patients visual acuity was less than 0.1 in at least one eye. The degree of retinopathy was found to be related to the duration of diabetes mellitus, age at onset, glycaemic control (HbA1c), blood pressure and symptoms of neuropathy. CONCLUSIONS: The prevalence of retinopathy of 22.0% in the study group was found to be low for non-proliferative diabetic retinopathy, perhaps due to the methods used and/or good or acceptable glycaemic control measured as HbA1c.

Adult↗
PubMed2000

[The sonographic picture of an echogenic liver is an indicator of pathologic glucose tolerance].

BACKGROUND: Almost all patients in departments of internal medicine routinely undergo abdominal ultrasound examination in which liver changes indicating hepatic steatosis are often detected. The aim of this study was to assess the occurrence of pathological oral glucose tolerance, manifest diabetes mellitus and other changes indicative of a metabolic syndrome in patients with sonographic signs of hepatic steatosis. PATIENTS AND METHODS: 577 patients were examined during a period of 6 months: 90 patients fulfilled the inclusion criteria. RESULTS: Among the 90 patients with echodense liver who were included in the study (42 female, 48 male) 36 patients presented with previous diagnosis of diabetes mellitus (40%). The oral glucose tolerance test was impaired in 19 patients (21%) and in four patients with manifest diabetes mellitus (4%). Among patients with echodense liver a high percentage presented with obesity and impaired fat metabolism. CONCLUSIONS: The large number of patients with an impaired oral glucose tolerance test converting to manifest diabetes, as well as the large number of patients with manifest disorders of fat metabolism suggest that screening for diabetes should be performed in patients who present with sonographic signs of hepatic steatosis.

Adolescent↗
PubMed2000

Amelioration of hyperglycemic and hyperosmotic induced vascular dysfunction by in vivo inhibition of protein kinase C and p38 MAP kinase pathway in the rat mesenteric microcirculation.

BACKGROUND: Recently, we demonstrated in vivo effects of acutely induced hyperglycemia, diabetes and mannitol infusions on rat mesenteric microcirculation concerning leukocyte-endothelial-cell interaction (Schäffler et al. EJCI 28: 886-893, 1998). DESIGN: In this study we have investigated the possible involvement of the protein kinase C (PKC) and p38 MAP kinase cascade as signal transducing elements during hyperglycemic and osmotic stress in an in vivo rat model. RESULTS: Acutely induced hyperglycemia resulted in a significant increase in leukocyte adhesion. This effect could be mimicked by mannitol. Both PKC and p38 MAP kinase were involved in the effects mediated by glucose and mannitol. Acutely induced hyperglycemia resulted in a significant increase in leukocyte emigration. This effect could be imitated by mannitol. However, PKC and p38 MAP kinase were only involved under osmotic stimulation. The hyperglycemia-induced reduction in leukocyte rolling velocity seemed to be a glucose-specific effect, since mannitol did not influence leukocyte rolling velocity. This glucose effect on leukocyte rolling velocity was mediated by an activation of the PKC/p38 MAP kinase cascade. Both hyperglycemia and osmotic stimuli alone were able to reduce venular shear rate without recruitment of the p38 MAP kinase cascade. The observed reduction of shear rate seems to be mediated only by the osmotic effects of glucose via activation of the PKC system. CONCLUSION: The observed effects of glucose on adhesion, emigration and shear rate are due to osmotic effects. The PKC/MAP kinase cascade is involved as a signal transducing component. The reduction of leukocyte rolling velocity is a glucose-specific effect, mediated by the activation of both the PKC and the p38 MAP kinase cascade. Venular shear rate and leukocyte emigration can be influenced by glucose and mannitol due to different regulation mechanisms. It is concluded, that isoform-specific inhibitors of PKC and specific MAP kinase inhibitors represent a potential drug target for preventing microvascular dysfunction in diabetes.

Animals↗
PubMed2000

Mutation analysis of the human adipocyte-specific apM-1 gene.

BACKGROUND: The aim of this study was to analyse the human adipocyte-specific apM-1 gene for sequence variations. METHODS: Sequence analysis was performed in 344 randomly chosen blood samples using a capillary sequencer. RESULTS: Whereas no mutations were detected in intronic regions and in 2.7 kb of the promoter, two sequence variations were found within the coding sequence of apM-1. For both mutations, a polymerase chain reaction-(PCR) based restriction fragment length polymorphism (RFLP) analysis was developed, which provided a rapid screening method. A conservative T --> G transition at nucleotide + 45 within exon-2 [Gly15Gly] was detected with an allelic frequency of 0.9 for the wild-type allele and 0.1 for the mutated allele. In addition, a missense point mutation at nucleotide + 331 within exon-3 [Tyr111His] was detected with an allelic frequency of 0.97 for the wild-type allele and 0.03 for the mutated allele. This mutation replaces a tyrosine by an histidine within the carboxyterminal globular domain of apM-1. Concerning the Gly15Gly polymorphism, the TT genotype was found in 275 subjects (79.9%), the TG genotype in 67 subjects (19.5%) and the GG genotype in 2 subjects (0.6%): one with maturity onset diabetes of young age (MODY-diabetes) and one with Lipoatrophic Diabetes Syndrome (LPDS). Concerning the Tyr111His polymorphism, the TT genotype was found in 328 subjects (95.4%), the TC genotype in 15 subjects (4.3%) and the CC genotype in 1 subject (0.3%). CONCLUSION: The existence of two yet unknown mutations within the apM-1 gene was demonstrated and RFLP analysis was established for rapid screening. Well defined cohorts of patients are necessary to determine the putative role of apM-1 gene mutations in the pathogenesis of metabolic disorders.

Adipocytes↗
PubMed2000

Elevated levels of leptin and insulin but not of TNF alpha are associated with hypertension in type 2 diabetic males.

Leptin and TNF alpha are thought to influence blood pressure. Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. In 424 type 2 diabetic patients (79 hypertensive females [+Hf], 79 normotensive females [-Hf]; 133 hypertensive males [+Hm], 133 normotensive males [-Hm]) matched for sex, age and BMI serum leptin levels were measured by RIA and TNF alpha, insulin, estradiol, progesterone by ELISA as well as free testosterone by RIA. Leptin levels were comparable in +Hf and -Hf (16.5 +/- 1.0 microg/l vs 16.3 +/- 1.0 microg/l) but higher in +Hm as compared to -Hm (8.3 +/- 0.47 microg/l vs 6.5 +/- 0.34 microg/l; p<0.05). In addition, in comparison to -Hm serum levels of insulin (190 +/- 10 pmol/l vs 161 +/- 11 pmol/l; p< 0.005) and also of creatinine (118.6 +/- 3.6 micromol/l vs 101.7 +/- 2.3; p< 0.0001) were higher in +Hm. Pearson's Correlation coefficient revealed a positive correlation between levels of leptin and diastolic blood pressure (p<0.05) and also between leptin and insulin (p<0.001) in males, however, only before correction for BMI. No correlation between leptin and creatinine was found in males and females. Levels of TNF alpha were comparable in all subgroups. No correlation between levels of TNF alpha and serum leptin levels, blood pressure and insulin was found. In females TNF alpha was positively correlated with creatinine (p<0.001) and in males positively with progesterone (p<0.001). Taken together, higher serum leptin levels were found in hypertensive type 2 diabetic males as compared to normotensives, which may be related to the BMI and higher levels of insulin. These findings are accompanied by a trend to lower levels of free testosterone in hypertensive type 2 diabetic males. TNF alpha levels were comparable in female and male hypertensive and normotensive type 2 diabetic subjects.

Aged↗
PubMed2000

Identification of a new missense mutation (Gly95Glu) in a highly conserved codon within the high-mobility group box of the sex-determining region Y gene: report on a 46,XY female with gonadal dysgenesis and yolk-sac tumor.

Leydig cells and Sertoli cells of the testes produce hormones that cause male differentiation, if receptors are present. The Y chromosomal SRY gene (sex determining Region Y gene) acts as TDF and is required for regular male sex determination. SRY represents a transcription factor belonging to the superfamily of genes sharing the HMG-box motif(high-mobility group-box), which acts as DNA binding region. Here, we describe a nonmosaic XY sex-reversed female with pure gonadal dysgenesis (46,XY karyotype, completely female external genitalia, normal Müllerian ducts, absence of Wolffian ducts, streak gonads) who harbored a yolk-sac tumor and was referred for the assessment of primary amenorrhea. Using genomic PCR analysis, a 423-bp PCR product, encompassing the HMG-box of the SRY gene, was amplified from the proposita, her father, and her three brothers, whereas no band was visible in the patient's mother and her three sisters. The PCR products were sequenced for mutations subsequently. A new de novo missense mutation within the HMG-box of the SRY gene was discovered in the proposita. A G is replaced by an A in codon 95 at position +284, resulting in the replacement of the nonpolar aminoacid glycine by the polar amino acid glutamate. The glycine at codon 95 is highly conserved between the family of HMG-box proteins and between species. This point mutation has not been described earlier and brings the total number of SRY mutations described so far to 36, each mutation being unique. This mutation was not detected in the patient's father and her male siblings. The present data provide further evidence to support the functional importance of the putative DNA binding activity of the SRY HMG-box domain.

Adult↗
PubMed2000

A 30 year history of panniculitis.

The differential diagnosis of panniculitis may be challenging due to the uniform clinical presentation of different panniculitis subsets. We describe a 45-year-old woman with a 30 year history of panniculitis, who had repeatedly failed to fulfill diagnostic criteria for various panniculitis subsets. Finally, erythema induratum was diagnosed and she was successfully treated with antituberculous chemotherapy. The wide spectrum of histological alterations of chronic erythema induratum as well as the sensitivity of polymerase chain reaction for Mycobacterium tuberculosis in erythema induratum lesions is discussed.

Antitubercular Agents↗
PubMed1999

[Giant fecaliths in habitual constipation].

HISTORY AND FINDINGS: A 17-year old adolescent with chronic constipation developed fecal incontinence with liquid, fetid stool. He had had variable bowel symptoms since early childhood, but not in his infancy. Since several years he had undergone psychotherapeutic treatment for depression due to a familial conflict situation. Abdominal palpation revealed the presence of a large, hard mass in the lower abdomen, measuring about 20 cm in diameter. INVESTIGATIONS: A defecography verified the presence of a huge obstructing fecalith in the rectum, with massive dilation and elongation of the antecedent rectum and colon (megarectum and megacolon). Neither endoscopy nor radiological imaging revealed a narrow bowel segment. In sequential biopsies, no indication of aberrant innervation was found. The recto-anal inhibitory reflex could be elicited. TREATMENT AND COURSE: Restoration of the rectal passage was achieved by manual disimpaction in numerous sessions, supported by repeated rectal enemas. Subsequently, the patient had normal daily bowel movements for a few days. However, he had to be readmitted three weeks later because again a fecalith had formed, measuring 15 cm in diameter. A few days after discharge the patient hat not followed the exhortation to void ad least once per day. After renewed disimpaction he was referred to a psychosomatic clinic. CONCLUSION: Voluntary withholding of defecation can eventuate massive coprostasis and the development of megacolon and megarectum. In theses instances the major complaint may not be constipation but paradoxical diarrhea. A number of conditions have to be excluded before the diagnosis idiopathic megacolon can be confirmed. Treatment ist difficult and often necessitates prolonged and repetitious interventions.

Adolescent↗