Biomedical Engineering Reference
In-Depth Information
paracrine as well as an autocrine factor (Friedman
2002
; Hall et al.
2002
) . The upregulation of
leptin expression in adipose cells from heat shock
indicates that leptin helps in the thermoregula-
tory processes to limit body hyperthermia by a
central action that is responsible for the decrease
in feed intake, energy metabolism and body fat
(Houseknecht et al.
1998
) . Adipocytes have been
observed to express leptin receptors indicating
that leptin may act directly on adipocytes for regu-
lating energy and metabolism. This indicates that
two regulatory systems 'short-loop' leptinergic
system and hypothalamic 'long-loop' energy reg-
ulatory systems independently exist (Wang et al.
2005
). The leptin in severe heat-shocked cells
induces adipocyte apoptosis (Ambati et al.
2007
) .
Leptin changes in severe heat-shocked 3T3-L1
adipocytes might indicate a proapoptotic signal
of leptin (Bernabucci et al.
2009
) . The increase
of leptin expression may be a consequence of a
possible adaptative response to heat shock and
downregulation of adiponectin might be a cell
heat-shock response that is accompanied by a
reduction in protein synthesis to favour induction
of heat-shock response (Linquist
1986
; Collier
et al.
2006b
) .
Adiponectin has a potent anti-inflammatory
effect and leptin exerts a proinflammatory role
(Fantuzzi
2005
). The upregulation of leptin and
downregulation of adiponectin determine the
alteration of energy and lipid metabolism observed
in cattle exposed to hot environment (Bernabucci
et al.
2009
; Ronchi et al.
1999
) . The downregula-
tion of adiponectin and upregulation of leptin are
comparable with the regulation of adipokines
observed in humans having obesity, atherosc-
lerosis, diabetes type 2 and metabolic syndrome
(Kamigaki et al.
2006
; Lafontan and Viguerie
2006
). Altered adipokine levels also occur in a
variety of inflammatory conditions (Fantuzzi
2005
). Hsps have role in the inflammatory
response and participate in cytokine signal trans-
duction and in the control of cytokine gene
expression (Moseley
1998
) . Therefore, changes
of adipokine gene and protein expression and
Hspa2
gene expression observed in heat-
shocked adipocytes might be responsible for a
proinflammatory response associated to insulin
resistance (Ailhaud
2006
) and CVD (Fantuzzi
2005
) in heat-stressed humans. Studies need to be
undertaken to verify whether heat-shock-induced
impairment of adipokines are similar to humans
and in livestock and affect energy balance in
animals during metabolic diseases and heat stress.
In vivo studies are necessary in high-producing
cows to confirm the association between adi-
pokine expression and heat stress.
Reduced leptin and/or Ob-Rb expression in heat-
shocked lymphocytes may represent an adaptive
mechanism to high environmental temperatures,
which may contribute to explain the immunosup-
pression that may take place in cows suffering from
severe heat stress (Lacetera et al.
2009
) .
9
Reproductive Hormones
9.1
FSH and LH
Ovarian activity is primarily regulated by gona-
dotrophins released from pituitary under the
influence of gonadotrophin-releasing hormone
from the hypothalamus. The release of luteinising
hormone (LH) and follicle-stimulating hormone
from the anterior pituitary gland is disrupted by
heat stress. Therefore, heat stress has a detrimental
effect on reproduction partly by disrupting the
normal release of these hormones (Dobson et al.
2003
). The effect of heat stress on LH concentra-
tions in peripheral blood has been observed to be
inconsistent. Gwazdauskas et al. (
1981
) and
Gauthier (
1986
) reported unchanged concentra-
tions, while Roman-Ponce et al. (
1981
) reported
increased concentrations and some authors
reported decreased concentrations (Madan and
Johnson
1973
; Wise et al.
1988a
) in heat-stressed
cows. These discrepancies may be associated
with differences in sampling frequency, which
varied from once a day to once every 3 h and
depended on whether heat stress was acute or
chronic. Regarding the pattern of LH secretion in
heat-stressed cows, Gilad et al. (
1993
) found
lower LH basal concentrations and lower LH
amplitude in heat-stressed cows with low plasma
oestradiol, and Wise et al. (
1988a
) found lower
LH pulse frequency in the heat-stressed cows
