Higher ADPN and lower WHRs (higher peripheral adiposity) are associated with better metabolic health in both nonobese and obese white individuals. These results suggest that ADPN and peripheral adiposity play a key role in determining the metabolic health independent of body mass index.
Thirty percent of obese individuals are metabolically healthy and were noted have increased peripheral obesity. Adipose tissue is the primary source of adiponectin, an adipokine with insulin-sensitizing and anti-inflammatory properties. Lower adiponectin levels are observed in individuals with obesity and those at risk for cardiovascular disease. Conversely, higher levels are noted in some obese individuals who are metabolically healthy. Our objective was to determine whether abdominal adiposity distribution, rather than BMI status, influences plasma adiponectin level. Four-hundred and twenty-four subjects (female: 255) of Northern European ancestry were recruited from “Take Off Pounds Sensibly” (TOPS) weight loss club members. Demographics, anthropometrics, and dual X-ray absorptiometry of the whole body and CT scan of the abdomen were performed to obtain total body fat content and to quantify subcutaneous adipose tissue and visceral adipose tissue respectively. Laboratory measurements included fasting plasma glucose, insulin, lipid panel, and adiponectin. Age- and gender-adjusted correlation analyses showed that adiponectin levels were negatively correlated with body mass index, waist circumference, triglycerides, total fat mass, and visceral adipose tissue. A positive correlation was noted with HDL-cholesterol and fat free mass (p<0.05). Subcutaneous adipose tissue -to-visceral adipose tissue ratios were also significantly associated with adiponectin (r=0.13, p = 0.001). Further, the best positive predictors for plasma adiponectin were found to be subcutaneous adipose tissue -to-visceral adipose tissue ratios and gender by regression analyses (P<0.01). Abdominal adiposity distribution is an important predictor of plasma adiponectin and obese individuals with higher subcutaneous adipose tissue -to-visceral adipose tissue ratios may have higher adiponectin levels.
The corticosterone response to acute hypoxia in neonatal rats develops in the 1st wk of life, with a shift from ACTH independence to ACTH dependence. Acute hypoxia also leads to hypothermia, which may be protective. There is little information about the endocrine effects of body temperature maintenance during periods of neonatal hypoxia. We hypothesized that prevention of hypothermia during neonatal hypoxia would augment the adrenocortical stress response. Rat pups separated from their dams were studied at postnatal days 2 and 8 (PD2 and PD8). In one group of pups, body temperature was allowed to spontaneously decrease during a 30-min prehypoxia period. Pups were then exposed to 8% O(2) for 3 h and allowed to become spontaneously hypothermic or externally warmed (via servo-controlled heat) to maintain isothermia. In another group, external warming was used to maintain isothermia during the prehypoxia period, and then hypoxia with or without isothermia was applied. Plasma ACTH and corticosterone and mRNA expression of genes for upstream proteins involved in the steroidogenic pathway were measured. Maintenance of isothermia during the prehypoxia period increased baseline plasma ACTH at both ages. Hypothermic hypoxia caused an increase in plasma corticosterone; this response was augmented by isothermia at PD2, when the response was ACTH-independent, and at PD8, when the response was ACTH-dependent. In PD8 rats, isothermia also augmented the plasma ACTH response to hypoxia. We conclude that maintenance of isothermia augments the adrenocortical response to acute hypoxia in the neonate. Prevention of hypothermia may increase the stress response during neonatal hypoxia, becoming more pronounced with increased age.
One of the biggest challenges of premature birth is acute hypoxia. Hypothermia during acute hypoxic periods may be beneficial. We hypothesized that prevention of hypothermia during neonatal hypoxia disrupts glucose homeostasis and places additional metabolic challenges on the neonate. Pups at PD2 and PD8 were exposed to 8% O2 for 3 h, during which they were allowed to either spontaneously cool or were kept isothermic. There was also a time control group that was subjected to normoxia and kept isothermic. Plasma glucose, insulin, C-peptide, corticosterone, and catecholamines were measured from samples collected at baseline, 1 h, 2 h, and 3 h. In postnatal day 2 (PD2) rats, hypoxia alone resulted in no change in plasma glucose by 1 h, an increase by 2 h, and a subsequent decrease below baseline values by 3 h. Hypoxia with isothermia in PD2 rats elicited a large increase in plasma insulin at 1 h. In PD8 rats, hypoxia with isothermia resulted in an initial increase in plasma glucose, but by 3 h, glucose had decreased significantly to below baseline levels. Hypoxia with and without isothermia elicited an increase in plasma corticosterone at both ages and an increase in plasma epinephrine in PD8 rats. We conclude that the insulin response to hypoxia in PD8 rats is associated with an increase in glucose similar to an adult; however, insulin responses to hypoxia in PD2 rats were driven by something other than glucose. Prevention of hypothermia during hypoxia further disrupts glucose homeostasis and increases metabolic challenges.
Apnea due to immature respiratory control is a common cause of neonatal intermittent hypoxia (IH). We hypothesized that IH disrupts glucose homeostasis and is a metabolic stressor. Rats at postnatal days (PD) 2–3, 7–8, or 11–12 were exposed to 6 @ 30‐sec cycles of IH (3% O2) over 1 hr. An additional group of PD7‐8 pups underwent IH for 3 cycles over 0.5 hr, but were pretreated (on PD3, 5, and 6) with guanethidine (chemical sympathectomy). In PD2‐3 rats, plasma glucose, insulin, and C‐peptide were increased at the 6th cycle of IH. In PD7‐8 rats, plasma glucose, insulin, and C‐peptide increased by the 3rd cycle, but by the 6th cycle, glucose had returned to baseline. PD11‐12 pups experienced a similar increase in plasma glucose, but a much larger increase in insulin and C‐peptide compared to PD7‐8. IH caused bradycardia and a decrease in body temperature. Pretreatment with guanethidine in PD7‐8 rats augmented the increase in insulin and C‐peptide; heart rate at baseline, and heart rate and body temperature at their nadirs during IH were lower after guanethidine pretreatment. We conclude that IH alters glucose homeostasis and induces bradycardia in neonates. The sympathetic nervous system restrains the insulin response and maintains heart rate during IH in the neonate.
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