Search

The diagnosis of the metabolic syndrome (MS) according to the National Cholesterol Education Program Adult Treatment Panel III does not reflect necessarily the presence of insulin resistance (IR), a potential therapeutical target for type 2 diabetes and cardiovascular disease prevention. Based on previous prevalence data, a cross-sectional study was conducted to determine the HOMA-IR relationship to the MS and some associated abnormalities. HOMA-IR > was higher in individuals with the MS (2.8+/-1.6 vs. 1.8+/-1.4) (p < 0.001). HOMA-IR >or= 2.5 allied good specificity and sensitivity levels for the association of MS and IR. Hyperglycemia, hypertrigliceridemia, and abdominal obesity, the MS components best related to IR, were statistically associated with HOMA-IR > 2.5, but not hypertension neither low HDL-c. The demonstration that some of MS phenotypes or associated abnormalities were more predictive for IR could point out to the possibility of the use of the index as a marker of the presence of IR associated to MS.

Male Wistar rats (N = 84) weighing 230-270 g were fasted 48 hr. Equal groups were controls, nephrectomized bilaterally and sham-operated. Equal subgroups were then given 4.0, 6.0 or 7.5 g of alcohol per kg of body weight or water by orogastric intubation. Blood glucose levels did not decrease significantly after nephrectomy alone or after the 4.0 g/kg dose. Blood glucose declined significantly more in the nephrectomized than in the sham-operated rats at 90 and 180 min after the 6.0 g/kg dose. Blood glucose decreased significantly in both the nephrectomized and sham-operated rats after the 7.5 g/kg dose.

The potential of ethanol-induced hypothermia on the glycemic alterations induced by this drug were evaluated. In Experiment 1 ambient temperature was manipulated. After 4.0 g/kg of ethanol blood glucose levels and body temperature were assessed in fed or 48 hr starved rats at either 21 degrees C or 28 degrees C room temperature. Hyper or hypoglycemia was observed depending on both the feeding condition and the environmental temperature. In Experiment 2, this hypothesis was tested by determining if rats tolerant to the thermic effects of ethanol would show a decreased glycemic response. The results support this assumption.

The effects of 1.0, 3.0 and 5.0 g/kg of ethanol on blood glucose levels and body temperature were examined in rats submitted to either acute food deprivation (24 or 48 hr), chronic starvation, or to both chronic plus acute food deprivation. The results show that: (a) 3.0 and 5.0 g/kg produced either an increase or a decrease of glucose levels depending on the state of fasting; (b) rats not deprived of food presented hyperglycemia while being hypothermic; (c) a marked hypothermia was present when no substantial alterations in glycemia were observed; and (d) in cases where hypoglycemia and hypothermia occurred, the fall in body temperature paralleled or preceded the decrease in glucose levels.

The influence of pretreatment with 5.0 or 10.0 mg/kg of indomethacin, a prostaglandin synthetase inhibitor, on the alterations in body temperature produced by 3.0 and 4.0 g/kg of ethanol, was studied in food-deprived and free-feeding rats. A partial antagonism of ethanol's hypothermic effect resulted from indomethacin pretreatments and this effect was found to be ethanol dose-dependent. This result could account for the conflicting reports in the literature on the effectiveness of indomethacin in antagonizing ethanol-induced hypothermia. Indomethacin (5.0 mg/kg) also antagonized ethanol-induced hypoglycemia in 48 hr starved rats. The relationship between two effects of ethanol, hypothermia and hypoglycemia, is discussed.

An experiment was undertaken to characterize the influence of ambient temperature on ethanol-induced glycemic alterations in rats. Animals under two different feeding conditions (nonfasted or 48-hr fasted) were IP injected with 4.0 g/kg of ethanol. Blood glucose and body temperature were measured before, 90 and 180 min after drug administration. The rats were tested under ambient temperatures of 16, 21 and 32 degrees C. Fed animals with a mean pre-drug glycemia of near 105 mg/100 ml presented a variation of blood glucose ranging from 50 mg/100 ml at 16 degrees C to 140 mg/100 ml at 32 degrees C. The glycemia from fasted rats, with a starting value of 70 mg/100 ml ranged from 20 to 115 mg/100 ml at 16 and 32 degrees C, respectively. It was concluded that the administration of ethanol can render nonfasted as well as fasted rats hypo or hyperglycemic, depending upon the environmental temperature.