Effects of Restricted Fructose Access on Body Weight and Blood Pressure Circadian Rhythms

High-fructose diet is known to produce cardiovascular and metabolic pathologies. The objective was to determine whether the timing of high fructose (10% liquid solution) intake affect the metabolic and cardiovascular outcomes. Male C57BL mice with radiotelemetric probes were divided into four groups: (1) 24 h water (control); (2) 24 h fructose (F24); (3) 12 h fructose during the light phase (F12L); (4) 12 h fructose during the dark phase (F12D). All fructose groups had higher fluid intake. Body weight was increased in mice on restricted access with no difference in total caloric intake. Fasting glycemia was higher in groups with restricted access. F24 mice showed a fructose-induced blood pressure increase during the dark period. Blood pressure circadian rhythms were absent in F12L mice. Results suggest that the timing of fructose intake is an important variable in the etiology of cardiovascular and metabolic pathologies produced by high fructose consumption

Screening Assay for Enzymes Involved in Pathophysiology Using SELDI-TOF Mass Spectrometr

The invention provides methods for quantifying enzymatic activity of an enzyme with a known substrate. The methods employ SELDI-TOF mass spectrometry, and are suitable, in particular, for assaying aspects of the renin-angiotensin system. The methods may be utilized to assess and/or monitor biological conditions associated with the renin-angiotensin system prior to the manifestation of known physiological and biomarkers for such conditions. The methods are suitable for analysis of pharmacological effectors of the renin-angiotensin system, and are particularly suitable for automation and high-throughput screening assay design

Screening Assay for Inhibitors of Severe Acute Respiratory Syndrome (SARS) Using SELDI-TOF Mass Spectrometry

Mass spectrometric methods directed to screening libraries of compounds for agents that inhibit entry of Severe Acute Respiratory Syndrome (SARS) coronavirus (CoV) into cells are provided, along with methods for comparatively evaluating inhibitors of the SARS CoV

Phosphoglycan Messengers and Their Medical Uses (Lipidemia)

Phosphoglycan messengers (PGMs) which are carbohydrate derivatised phosphatidyl cyclitols are disclosed, together with the finding that these substances are biologically active, e.g. in lowering blood glucose levels. These compounds are distinct from GPI-anchors disclosed in the prior art as these GPI-anchors are protein linked and are not biologically active

Hypoglycemia and Hyperinsulinemia in Rodent Models of Severe Malaria Infection

Severe hypoglycemia developed during nonlethal Plasmodium chabaudi and lethal P. yoelii blood stage malaria infection in mice, always in association with hyperinsulinemia. Supernatants of lethal P. yoelii incubated overnight induced hypoglycemia and hyperinsulinemia in normal mice. In murine malaria, hypoglycemia may be largely secondary to increased insulin secretion

Screening Assay for Enzymes Involved in Pathophysiology Using SELDI-TOF Mass Spectrometr

The invention provides methods for quantifying enzymatic activity of an enzyme with a known substrate. The methods employ SELDI-TOF mass spectrometry, and are suitable, in particular, for assaying aspects of the renin-angiotensin system. The methods may be utilized to assess and/or monitor biological conditions associated with the renin-angiotensin system prior to the manifestation of known physiological and biomarkers for such conditions. The methods are suitable for analysis of pharmacological effectors of the renin-angiotensin system, and are particularly suitable for automation and high-throughput screening assay design

Treatment of Diabetes

The present invention provides methods for using a killed malaria parasite or an extract thereof in the treatment of non-insulin dependent diabetes mellitus (NIDDM)

Screening Assay for Inhibitors of Severe Acute Respiratory Syndrome (SARS) Using SELDI-TOF Mass Spectrometry

Mass spectrometric methods directed to screening libraries of compounds for agents that inhibit entry of Severe Acute Respiratory Syndrome (SARS) coronavirus (CoV) into cells are provided, along with methods for comparatively evaluating inhibitors of the SARS CoV

Acute stress-induced hyperinsulinemia in the pertussis toxin-treated rat: Possible role of humoral β-cell-tropic factors

The present study was undertaken to determine if acute stress induced by exposure to ether resulted in the presence of β-cell-tropic factors in rat plasma and if this insulinotropic activity was increased by pertussis toxin. Rats pretreated with pertussis toxin (5 μg/kg, 5 days previously) showed marked hyperinsulinemia, but only after exposure to ether before blood sampling. This hyperinsulinemia was not modified by adrenal demedullation. Effects on insulin secretion were assessed by incubation of plasma (diluted with Krebs buffer) with collagenase-isolated rat pancreatic islets. When blood was collected by decapitation from normal rats, the subsequently prepared plasma (12.5% to 50%) profoundly inhibited insulin release from rat isolated islets. This inhibition was probably mediated by catecholamines, since it was not seen with plasma from adrenal-demedullated rats and was prevented by α2-adrenoceptor-blocking drugs. Plasma from adrenal-demedullated, pertussis toxin-treated rats stimulated insulin secretion (by 60%) when the donor rats had been exposed to ether before blood sampling. It is suggested that stress may result in the presence of circulating β-cell-tropic factors, which may contribute to the acute stress-induced hyperinsulinemia seen in pertussis toxin-treated animals

Phosphoglycan Messengers and Their Medical Uses (SLE)

PPhosphoglycan messengers (PGMs) which are carbohydrate derivatised phosphatidyl cyclitols are disclosed, together with the finding that these substances are biologically active, especially in modulating plasma cholesterol, plasma triglycerides and/or high density lipoprotein levels and/or modulating the LDL:HDL ratio, and for the treatment of lipodystrophy or dyslipidemia. These compounds are distinct from GPI-anchors disclosed in the prior art as these GPI-anchors are protein linked and are not biologically active