amyloid/obesity

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Islet amyloid-associated diabetes in obese A(vy)/a mice expressing human islet amyloid polypeptide.

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We have previously shown that hemizygous transgenic mice expressing human islet amyloid polypeptide (hIAPP) in pancreatic beta-cells have no diabetic phenotype, whereas in the homozygous state, they developed severe, early-onset hyperglycemia associated with impaired insulin secretion and beta-cell

Intrahippocampal administration of a domain antibody that binds aggregated amyloid-β reverses cognitive deficits produced by diet-induced obesity.

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BACKGROUND The prevalence of high fat diets (HFD), diet-induced obesity (DIO) and Type 2 diabetes continues to increase, associated with cognitive impairment in both humans and rodent models. Mechanisms transducing these impairments remain largely unknown: one possibility is that a common mechanism

Amyloid precursor protein expression is upregulated in adipocytes in obesity.

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The aim of this study was to determine whether amyloid precursor protein (APP) is expressed in human adipose tissue, dysregulated in obesity, and related to insulin resistance and inflammation. APP expression was examined by microarray expression profiling of subcutaneous abdominal adipocytes (SAC)

Insulin resistance syndrome and Alzheimer's disease: age- and obesity-related effects on memory, amyloid, and inflammation.

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Insulin plays an important role in memory and other aspects of brain function. The insulin resistance syndrome, characterized by chronic peripheral insulin elevations, reduced insulin activity, and reduced brain insulin levels, is associated with age-related memory impairment and Alzheimer's disease

Estrogen can prevent or reverse obesity and diabetes in mice expressing human islet amyloid polypeptide.

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Type 2 diabetes is characterized by loss of beta-cell mass and concomitant deposition of amyloid derived from islet amyloid polypeptide (IAPP). Previously we have shown that expression of human IAPP (huIAPP) in islets of transgenic mice results in either a rapid onset of hyperglycemia in mice

Serum Amyloid A concentration is increased in obese children and adolescents.

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OBJECTIVE To compare the circulating concentrations of the acute-phase protein serum amyloid A (SAA) in lean, overweight, and obese children and adolescents and analyze the influence of body fat. METHODS A total of 63 children and adolescents (65% girls) with an average age of 12.1 +/- 2.7 years

AA amyloidosis associated with morbid obesity (clinical case).

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We present the case of a 45-year-old woman who was hospitalized due to severe macrocytic anemia and renal failure. The patient presented a morbid obesity. The immunological study showed anti-ENA anti-SSA (Ro52) positive, with negative antinuclear antibodies. Also in the proteinogram (serum

Amyloidosis in ageing obese-hyperglycemic mice and their lean litter-mates. A morphological study.

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The occurrence of amyloidosis in obese-hyperglycemic mice (genotype obob) about 18 months old and their lean litter-mates was studied. Amyloidosis of varying degrees was found in 60 per cent of the mice and was equally common in both groups. Large amounts of amyloid were usually seen in the adrenal

Renal AA amyloidosis secondary to morbid obesity?

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Systemic amyloidosis is characterized by extracellular deposits on different organs of insoluble fibrils compounded of low molecular weight subunits coming from a great diversity of serum proteins. Secondary amyloidosis AA is due to fibril deposition composed of fragments of the acute phase reactant

Characterization of amyloid of ageing obese-hyperglycaemic mice and their lean littermates.

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Amyloid fibrils, isolated from 18-month-old obese-hyperglycaemic mice and their lean littermates, were characterized immunologically and chemically. The main amyloid fibril subunit protein was protein AA, which cross-reacted completely with an antiserum against amyloid from mice with experimentally

Islet amyloid polypeptide/amylin contents in pancreata increase in genetically obese and diabetic mice.

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To search for a possible relationship between islet amyloid polypeptide (IAPP)/amylin and the pathophysiology of type 2 diabetes mellitus, we examined IAPP contents in the pancreata of genetically obese and diabetic mice (C57BL/6J ob/ob and KK mice), at 24 weeks of age, using a specific

A novel oxidized low-density lipoprotein marker, serum amyloid A-LDL, is associated with obesity and the metabolic syndrome.

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BACKGROUND The putative association between the novel oxidized low-density lipoprotein markers, serum amyloid A-LDL (SAA-LDL) and alpha1-antitrypsin-LDL (AT-LDL), and obesity and the metabolic syndrome (MetS) has not been previously studied. In the present report, we investigated the levels of

Islet amyloid polypeptide/amylin contents in pancreas change with increasing age in genetically obese and diabetic mice.

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To search for a possible relationship between islet amyloid polypeptide (IAPP)/amylin and the pathophysiology of non-insulin-dependent (type 2) diabetes mellitus (NIDDM), we examined the changes in IAPP contents in the pancreata of genetically obese and diabetic mice (C57BL/6J ob/ob and C57BL/KsJ

Bace1-dependent amyloid processing regulates hypothalamic leptin sensitivity in obese mice.

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Obesity places an enormous medical and economic burden on society. The principal driver appears to be central leptin resistance with hyperleptinemia. Accordingly, a compound that reverses or prevents leptin resistance should promote weight normalisation and improve glucose homeostasis. The protease

Hypersecretion of islet amyloid polypeptide from pancreatic islets of ventromedial hypothalamic-lesioned rats and obese Zucker rats.

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To investigate the possible role of islet amyloid polypeptide (IAPP) in the development of type 2 diabetes mellitus, we examined the IAPP content and secretion in pancreatic islets isolated from ventromedial hypothalamic (VMH)-lesioned rats and genetically obese Zucker rats, using a specific RIA for

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