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T J Yost

Publications and source records attributed to T J Yost.

25 records · Page 2Linked to original sources
PubMed1988

Fat calories may be preferentially stored in reduced-obese women: a permissive pathway for resumption of the obese state.

We previously demonstrated in unpaired studies that corn oil ingestion at the beginning of a euglycemic insulin clamp study decreased the responsiveness of gluteal adipose tissue lipoprotein lipase (ATLPL) to glucose/insulin in lean subjects. In this investigation, we performed paired euglycemic insulin clamp studies with glucose/insulin with or without oral corn oil in each of six lean [mean, 64 +/- 3 (+/- SE) kg] normal women and nine moderately obese (91 +/- 3 kg) women before and after 12.4 +/- 1.4-kg weight loss and 3 months of weight maintenance to determine if the inhibitory effect of fat calories existed in each of these states. In the obese women the fasting ATLPL activity [5.6 +/- 1.1 (+/- SE) neq FFA/10(6) cells.min] was greater than in the normal women (1.6 +/- 0.2) and did not change after weight loss and maintenance (5.0 +/- 0.7). As expected, in normal women corn oil ingestion diminished the responsiveness of ATLPL to glucose/insulin [change (delta), 0.2 +/- 0.2 vs. 3.3 +/- 0.8; P less than 0.02] during a 6-h euglycemic insulin (40 mU/m2.min) clamp. In obese women ATLPL activity did not change under either experimental condition (glucose/insulin with or without corn oil). However, after weight reduction ATLPL activity increased not only in response to glucose/insulin alone (delta, 7.7 +/- 2.4), but also in response to glucose/insulin when corn oil was ingested (delta, 7.9 +/- 2.8). Moreover, the response of ATLPL activity to glucose/insulin and corn oil was greater than that in lean women (P less than 0.05). Thus, in reduced-obese women not only did fasting ATLPL activity remain elevated and ATLPL responsiveness to glucose/insulin increase, but fat ingestion failed to blunt the ATLPL response. This inability of dietary fat to diminish the responsiveness of ATLPL to glucose/insulin and, therefore, the effect of the lipase on triglyceride deposition in adipose tissue could contribute to the resumption of the obese state that so commonly occurs after successful weight reduction.

Adipose Tissue↗
PubMed1988

Plasma lipolytic activity. Relationship to postheparin lipolytic activity and evidence for metabolic regulation.

Lipolytic activity was measured in human plasma without prior administration of intravenous heparin. Eluted from heparin-Sepharose in a barbital buffer containing 6 mg/ml heparin, plasma lipolytic activities in 20 subjects were distributed between hepatic triglyceride lipase (HTGL, mean +/- SE 60.6 +/- 4.6%) and extrahepatic lipoprotein lipase (LPL, 39.4 +/- 4.6%). Confirmation of the identities of HTGL and LPL was provided by inhibitory antisera. Preheparin LPL activity was absent in plasma from a patient with type I hyperlipoproteinemia. Both preheparin HTGL and LPL activities correlated with the respective activities measured in plasma obtained 15 min after intravenous injection of heparin (rs = + .774 and + .685, respectively; n = 12). Evidence for the metabolic regulation of preheparin lipases was provided by measurement of significant increases in LPL and HTGL activities after oral glucose ingestion. Overall, preheparin plasma HTGL and LPL activities may reflect ongoing lipoprotein lipolytic activity in tissue beds, and because these measurements do not require the administration of intravenous heparin, they should prove useful for additional studies of short-term regulation of the lipases.

Adult↗
PubMed1988

Deficiency of the insulin, glucose-mediated decrease in serum triglycerides in normolipidemic obese subjects.

The effects of a 6-h insulin, glucose infusion on lipid metabolism were compared in 29 normolipidemic obese and 20 control subjects. Alterations in serum triglycerides (TG), cholesterol, and high-density lipoprotein (HDL) cholesterol were similar within groups when either 40 or 120 mU/m2 per min of regular insulin were infused. Although changes in the HDL cholesterol responses to the insulin, glucose infusions were also similar in obese and control subjects, TG fell more in insulin, glucose-infused controls (35 +/- 4 mg/dl, means +/- s.e.m.) than obese subjects (23 +/- 3) (P less than 0.001). The rate and magnitude of the insulin, glucose-mediated fall in free fatty acids, however, were not different between the two groups. This diminished responsiveness of TG to an insulin, glucose infusion in normotriglyceridemic obese subjects is another manifestation of the insulin resistance of obesity.

Adult↗
PubMed1987

Weight reduction increases adipose tissue lipoprotein lipase responsiveness in obese women.

Lipoprotein lipase was measured in gluteal adipose tissue from nine obese (90.6 +/- 2.7 kg) women fasting and after the intravenous infusion of insulin and glucose before, immediately after, and 3 mo subsequent to a 14.0 +/- 1.8% (mean +/- SEM) weight reduction. Fasting adipose tissue lipoprotein lipase activity (ATLPL) decreased from 5.3 to 2.3 nEq FFA/10(6) cells per min (P less than 0.02) immediately after weight reduction, yet after weight maintenance, higher levels were again found (6.1 nEq FFA/10(6) cells per min). Although responsiveness of ATLPL to 40 mU/m2 per min of insulin infusion over 6 h was absent before weight loss, increases were seen immediately after weight loss (delta 0.8, P = 0.05) and more so (delta 7.7, P less than 0.01) after 3 mo. Moreover, whereas before weight loss the ATLPL response to ingested mixed meals (delta 0.9) was minimal, in the maintained reduced-obese state a marked increase was seen (delta 12.6, P = 0.02). Thus, because ATLPL is important to lipid filling in adipose tissue, the maintenance of high levels of fasting ATLPL and the increase in enzyme responsiveness in the reduced-obese state could play an important role in the resumption of the obese state, which so commonly follows weight reduction.

Adipose Tissue↗
PubMed1984

Fat feeding decreases insulin responsiveness of adipose tissue lipoprotein lipase.

The acute effect of fat feeding on the insulin-mediated stimulatory response of adipose tissue lipoprotein lipase (ATLPL) was examined in normal-weight subjects. After two days of isocaloric-formula feeding, subjects were divided into the following four groups: intravenous (IV) saline alone (sal) (n = 5), IV saline and 67 g of oral corn oil ingested at the outset of the infusion (sal/fat) (n = 5), IV insulin (40 mU/m2/min) and glucose to maintain euglycemia (ins/glu) (n = 9), and IV insulin and glucose and oral corn oil (ins/glu/fat) (n = 8). Triglycerides fell less in the ins/glu/fat group than in the ins/glu group (0 +/- 8% v 35 +/- 5%, means +/- SEM, at three hours, P less than 0.01; 15 +/- 8% v 43 +/- 6% at six hours, P less than 0.02). ATLPL in the sal and sal/fat groups did not change during the six-hour period. When the responsiveness of ATLPL was compared between ins/glu/fat subjects and ins/glu subjects, decreases were seen at both three and six hours (-0.3 +/- 3.0 v 15.1 +/- 5.4 nEq/g/min, P less than 0.05; 6.7 +/- 2.7 v 27.9 +/- 3.9 nEq/g/min, P less than 0.001). The glucose infusion rates needed to maintain euglycemia were also decreased by fat feeding, 229 +/- 18 v 287 +/- 20 mg/m2/min (P less than 0.05). Thus, fat feeding with insulin and glucose infusions diminishes the insulin responsiveness of ATLPL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1984

Insulin responsiveness of adipose tissue lipoprotein lipase is delayed but preserved in obesity.

Because increases in adipose tissue lipoprotein lipase (ATLPL) may be important in the pathogenesis of obesity, the response of ATLPL to insulin during maintenance of euglycemia was examined in 22 obese and 8 normal weight subjects. Basal levels of ATLPL per g fat tissue for the obese and control groups were 18.7 +/- 2.0 (+/- SEM) and 9.6 +/- 2.7 neq/g X min, respectively. Insulin and glucose infusion rapidly produced antilipolysis in both groups, as evidenced by large falls in FFA by 20 min. When the responses of ATLPL in absolute change from basal were compared between the obese and control groups, no significant differences were found. However, because of the higher baseline ATLPL values in the obese subjects, the percent change in ATLPL from basal was significantly blunted at the 80 (P = 0.02), 180 (P less than 0.05), and 360 (P = 0.005) min timepoints compared to those in the normal subjects. By 3 h into the infusion, the control group had a significant rise in ATLPL above the basal level (4.2 +/- 1.3 ngq/g X min; P = 0.01), whereas the obese group did not (2.3 +/- 1.9 neq/g X min; P = NS). However, by 6 h, the ATLPL per g response above baseline was significantly increased in both normal (19.2 +/- 6.5 neq/g X min; P = 0.01) and obese subjects (9.8 +/- 2.3; P less than 0.001). Because adipose cell size was greater in obese subjects, data were also expressed per 10(6) cells. Basal ATLPL per 10(6) cells [11.8 +/- 1.7 neq/10(6) cells X min (obese); 3.4 +/- 0.9 neq/10(6) cells X min (normal)] was a function of cell size (rs = 0.713; P less than 0.001), body mass index (rs = 0.565; P less than 0.005), and basal insulin levels (rs = 0.434; P less than 0.05). As with the ATLPL per g response, the increases in ATLPL per 10(6) cells above basal were significant at both the 3 and 6 h marks for the normal subjects, but only at the 6 h timepoint for the obese group. Both steady state insulin levels [342 +/- 24 microU/ml (obese); 251 +/- 27 microU/ml (normal)] and the glucose infusion rates needed to maintain euglycemia [319 +/- 23 mg/m2 X min (obese); 312 +/- 33 mg/m2 X min (normal)] did not correlate with changes in ATLPL. Thus, insulin responsiveness of ATLPL in obese subjects was delayed but preserved. This phenomenon may be important in maintenance of the obese state.

Adipose Tissue↗